Over the past 100 years, cardiovascular disease (CVD) has become a leading cause of mortality and morbidity in developed countries, and similar trends have occurred for chronic liver disease. Subsequent research also indicated that people with non-alcoholic fatty liver disease (NAFLD) had a twofold increased risk of CV events and that this risk was doubled in those with liver fibrosis. However, no validated CVD risk score specific for NAFLD patients has yet been validated, as traditional risk scores tend to underestimate the CV risk in NAFLD patients. From a practical perspective, identifying NAFLD patients and assessing severity of liver fibrosis when concurrent atherosclerotic risk factors are already established may serve as an important criterion in new CV risk scores. The current review aims to assess current risk scores and their utility for the prediction of CV events among patients with NAFLD. Obesity is a multifactorial relapsing disease, as defined by the International Classification of Disease . AccordiBeing overweight or obese is among the main risk factors for developing non-alcoholic fatty liver disease (NAFLD), which is considered to be the most prevalent chronic liver disease worldwide . NAFLD iHowever, a new concept is emerging that is known as metabolic-associated fatty liver disease (MAFLD), which is a heterogenous clinical entity. The diagnostic criteria of MAFLD requires the presence of metabolic risk factors in the setting of hepatic steatosis, includes individuals with other concomitant liver diseases, and excludes those with hepatic steatosis who do not fulfill the metabolic risk criteria . Large cThe majority of people with NAFLD will not develop liver fibrosis or cirrhosis, yet some studies argue that by 2030, NASH will become the leading cause of liver transplant in the USA . An analAs previously reported, chronic liver disease (CLD) and cardiovascular diseases (CVDs) are stealing the spotlight in current epidemiological trends concerning morbidity and mortality rates. CVDs, which include ischemic heart disease, acute myocardial infarction, and stroke, are the most common non-communicable diseases globally, responsible for an estimated 17.8 million deaths in 2017 ,17. As tIn this manuscript, we aimed to review current risk scores and their utility for the prediction of cardiovascular events among patients with NAFLD. In light of more recent discoveries, we performed a literature search between January 2012 and January 2023 on MEDLINE, EMBASE, Web of Science, Scopus, DDW.org, and ClinicalTrials.gov for English articles. The search terms used included, but were not limited to, “NAFLD”, “non-alcoholic fatty liver disease”, “risk scores”, “cardiovascular risk scores”, “cardiovascular risk factors”, “mortality prediction scores”, “cardiovascular risk assessment”, and “prediction models”. The cited articles were selected based on their relevance to the review objective.Whether liver disease in NAFLD confers any additional CV risk, or whether an increase in CV risk in NAFLD is due to associated CVD risk factors, is still a matter of avid discussion. Understanding whether the liver disease in NAFLD contributes to additional CVD risk is important, as it is plausible that treatment of the liver disease may reduce the overall risk of CVD above the treatment of NAFLD-associated risk factors . Recent Risk factors for NAFLD are quite diverse. Beginning with alterations of hepatic microvasculature, increased arterial stiffness, and distortion of sinusoidal patterns which leads to intrahepatic endothelial dysfunction  and activation of angiogenesis and vascular remodeling via VEGF, we can better understand the complex pathophysiological mechanisms behind an otherwise benign affliction . SystemiFurthermore, mitochondrial malfunction and disruption is one of the main mechanisms of liver and heart damage. This should not come as a surprise since mitochondria are crucial organelles involved in cellular metabolism and homeostasis of energy . Many elThere are multiple intricate underlying mechanisms by which NAFLD increases the risk of CVD . NAFLD iSystemic inflammation, endothelial dysfunction, plaque instability, IR, oxidative stress, and altered lipid metabolism are some of the mechanisms involved in the complex pathogenesis of NAFLD-CVD . The livVisceral adipose fat appears to have a strong independent positive correlation with liver fat. However, the mechanism linking visceral fat to CVD is related to IR, which is also associated with an increased CV risk and atherosclerosis . BesidesApolipoprotein-B-containing lipoproteins operate as damage-associated molecular patterns (DAMPs) that activate Toll-like receptors (TLRs) after being transported and oxidized within the subendothelial vascular wall . TriglycAs previously reported, vascular abnormalities and endothelial dysfunction are recognized as initial steps in disease progression in both CLD and CHD. Endothelial dysfunction is a complex process and is the foundation for atherosclerosis before plaque inflammation ,43. In aIR is another key metabolic feature of both cardiovascular and hepatic injury. Patients who have IR have a suppression of insulin’s effects, which causes the liver to continuously produce glucose . AdiposeThe genetic profile also contributes to disease outcome. Changes in the polymorphism of patatin-like phospholipase domain-containing 3 and transmembrane 6 superfamily member 2 are linked to an increased risk of liver steatosis, fibrosis, and cancer ,54. HoweWhile some cohort studies revealed that NAFLD patients may have increased cardiovascular mortality, other research was unable to support this idea. For instance, a recent meta-analysis by Targher et al. revealed that people with NAFLD had a 64% higher likelihood than those without NAFLD of having fatal or nonfatal cardiovascular events. Non-fatal events included myocardial infarctions requiring coronary revascularization, strokes, and angina pectoris. The findings of Wu et al. differ from those of Tagher et al. in that they did not find a clear connection between the presence of NAFLD and an increase in cardiovascular mortality .A distinct risk group can be identified in patients with NAFLD who also have concurrent T2DM, NASH, or advanced fibrosis (F3–F4) . NAFLD pHs-CRP is a non-specific and sensitive marker for detecting inflammation that was proposed for its potential to add predictive value in several chronic diseases . A folloThe prevalence of arterial hypertension in NAFLD patients ranges from 40 to 70%, and recent research has demonstrated that NAFLD is closely linked to an elevated risk of incident prehypertension and hypertension . People Patients with NAFLD are more likely to develop both clinical and subclinical atherosclerosis. Patients with NAFLD may also be more susceptible to the development of atherosclerotic CVD due to an imbalance in procoagulant factors . In addiPatients with NAFLD/NASH are more likely to have subclinical CVD and several other cardiovascular risk factors . A summaBecause of the inherent limitations of using risk scores based on conventional CV risk-factor-derived multivariable statistical models to identify at-risk patients, the current global risk prediction studies are imperfect even though they may contribute to describing, at least in part, the relationship between NAFLD and increased CV risk ,31. AddiWith varying degrees of severity in each stage of simple steatosis and NASH, NAFLD progresses differently . Except for more severe cases of NASH+ fibrosis, these stages are typically reversible ,16,19. CTo diagnose the NAFLD stage and the degree of NASH and fibrosis by histological examination, as well as to track the course of the illness, liver biopsy is currently the “gold standard” (accounting for possible errors caused by sampling variability) . CurrentNAFLD can develop in individuals who are not overweight. In recent years, emerging evidence has demonstrated that lean NAFLD is a progressive condition and that predominantly male patients with lean NAFLD exhibited some features of MetS and might have worse outcomes than obese-NAFLD . WhetherThe NAFLD Liver Fat Score has its origins in a Finnish population . InsulinThe fatty liver index is based on BMI, the AST/ALT ratio, and the existence of T2DM, and this measure evaluates MAFLD/NAFLD ,85,86,87The APRI (AST-to-Platelet Ratio Index) is another easy-to-use tool to quickly assess the presence of fibrosis. It has been validated for the identification of NAFLD and can identify advanced fibrosis in those with viral infection. APRI is regarded as a good predictor of progressive fibrosis in patients with NAFLD . NeverthAnother widely used score is the NAFLD fibrosis score. Age, glucose levels, BMI, albumin and platelet count, and AST/ALT ratio are the parameters used. This score is widely used to predict advanced fibrosis. Particularly, patients with NAFLD have reduced levels of albumin and albumin-binding function. A high score (>0.68) significantly increased the probability of death in MAFLD/NAFLD patients by four times . Even thIn addition to risk-stratifying methods based on fibrosis for the MAFLD/NAFLD spectrum, many authors have proposed non-invasive scoring systems as screening tools for liver disease. However, some healthcare experts continue to emphasize liver biopsy as the gold standard for diagnosis while arguing for a thorough characterization of biopsy indications. However, fatty liver index, APRI, fibrosis-4 index, and NAFLD fibrosis score, in contrast to other available risk scores, depend on commonly requested parameters, making them easier to utilize in daily clinical practice . AdditioAlthough NAFLD is a common disease, there are no approved therapies. As previously reported, the leading causes of death in patients with NAFLD are complications of cardiometabolic disease. Therefore, efforts are directed toward developing drugs that target both NAFLD and cardiometabolic risk factors. Currently, several therapeutic agents have been proposed and are under assessment . Given tThe causal bidirectional relationship between CVD and NAFLD is more tangible nowadays. Early clinical intervention in at risk patients could alter the disease course. Moreover, patients who share multiple cardiometabolic risk factors who are at risk for developing CV events should benefit from early clinical and therapeutic intervention. Current guidelines do not recognize NAFLD as an independent risk factor for CVD, despite recent research indicating NAFLD’s involvement in incident CVD. Improving patient safety requires a greater understanding of the biopsy-free scores that are available for staging. Both NAFLD and CVD are silent pandemics, which are constantly expanding, and they compel clinicians to look for alternate methods of screening, early detection, and follow-up. Prospective long-term studies with homogeneous diagnostic criteria, considering not only the presence but also the severity of NALFD, are necessary to test if this diagnosis can improve cardiovascular disease risk stratification. New and inclusive risk scores are needed to address complex patients who are at risk of developing either CV events or progression toward more advanced and irreversible liver disease with overall poor outcome. Emerging new therapies could change the face of NAFLD patients.