## 1 Introduction  
Psoriasis is a chronic autoimmune skin disease with a complex etiology involving various genetic and environmental factors. It is characterized by inflammation and altered epidermal differentiation, inflammatory cell infiltrate in the epidermis and dermis, and dilation of superficial dermal blood vessels leading to red lesional plaques and scaling. The prevalence of psoriasis on a global scale across countries from published studies varies between 0.09% and 11.4%, but in most developed countries, the prevalence ranges from 1.5% to 5% [1,2]. Almost 90% of individuals with psoriasis have the most common form of the disease, known as psoriasis vulgaris or plaque psoriasis, characterized by well-demarcated, erythemat plaques plaques with overlying, coarse scale. Other major subtypes of psoriasis include gutate psoriasis, which typically presents as the acute onset of numerous small, inflammatory plaques; pustular psoriasis, which may present as an acute, subacute, or chronic pustular eruption; and erythroderric psoriasis, which exhibits cutaneous erythema and scale involving most or all the body surface area. There is growing and emerging evidence that psoriasis patients have a higher prevalence of associated comorbid disease multiple comorbidities, including psoriatic arthritis, cardiovascular disease (CVD), metabolic syndrome, mental health conditions such as depression and anxiety, inflammatory bowel disease (IBD), and malignancies such as lymphoma [1,3]. Although psoriasis can affect all ages, early onset for females and males occur around the age of 16 and 22, respectively, and late onset is mostly around 60 years for females, compared to 57 years for males [4]. Family-based and population-based epidemiological studies support a clear genetic contribution to the development of psoriasis. Having a family history increases the risk of psoriasis. Studies on monozygotic twins have reported a 70% chance of one twin developing psoriasis compared to 20% for paternal twins [5; 6]. PSOR1 is the major susceptibility locus for psoriasis, encoding the gene variant HLA-Cw6. A majority of early onset patients (around 85%) carries this locus, compared to late onset patients (around 15%) [4; 7; 8]. HLA-Cw6 is associated with various aspects of psoriasis including genetic susceptibility, clinical manifestation, comorbidity, and treatment efficacy [8]. Around nine psoriatic susceptibility loci have been identified by genome-wide association studies (GWAS), revealing several genomic markers [9; 10; 11; 12]. From a large meta-analysis of GWAS, with a sample data of \(>\)39,000 individuals (including data from eight Caucasian cohorts), [PERSON] et al. identified 16 additional psoriasis susceptibility loci for psoriasis. This study increased the number of identified loci to 63 for European-origin individuals and also highlighted the role of NFxB and interferon pathways, thereby providing insights to the pathogenesis of psoriasis [13; 14]. Other studies have also mapped psoriasis susceptibility loci, including PSORS1 on 6p21.3, PSORS2 on 17q, PSORS3 on 4q, PSORS4 on 1 cen-q21, PSORS5 on 3q21, and PSORS6 on 19p13 [15]. Transcriptome profiling and gene expression studies in psoriasis can provides valuable insights to the molecular basis of the disease, detecting new biomarkers and therapeutic targets. Microarray and RNA sequencing are relevant tools to detect new mRNA transcripts and alternatively spliced forms [7; 16]. Most of the current disease management approaches for psoriasis and psoriatic arthritis (PsA) depends on clinical assessments, and are often not precise. Hence, a more precise approach, which takes into account an individual's variations in genes, proteins, environment, and lifestyle, will provide better insight to help design precise therapies, leading to better treatment outcome.