## 1 Introduction  
For decades, the relationship between infections and survival in lung cancer has been studied. There are isolated reports of patients who, after developing postoperative empyema, showed long survival. It was assumed that this was due to a possible relationship between immune system activation and its action against cancer cells [1,2]. However, these are very limited series with short-term follow-ups. It is reasonable to believe that an activated immune system could attack cancer cells. But, in the case of empyema, the immune response generated is nonspecific. This is performed against bacteria, not against cells. This represents a totally different activation pathway [3,4]. New series and reports, with longer follow-up and larger populations, have attempted to detect the relationship between inflammation, infection, and prognosis. However, this relationship has not been satisfactorily demonstrated. In fact, some of these reports show a deleterious relationship between postoperative empyema and prognosis in lung carcinoma [5]. The immune response is known to play a significant role in shaping the short- and medium-term prognosis of lung cancer patients [3]. In the context of surgery, the choice of surgical approach can notably affect immune system activation. Open surgery has been linked to increased levels of pro-inflammatory factors and proteins that may promote tumor growth [6, 7, 8, 9]. In contrast, minimally invasive surgery tends to result in reduced cytokine release, a more balanced immune profile, and the release of proteins with antitumor properties [10, 11, 12, 13]. In recent years, robotic-assisted surgery has been added as a new tool for minimally invasive surgery with similar results when compared to Video-Assisted Thoracic Surgery (VATS). This has been demonstrated in surgical terms, showing a similar rate of conversion and a similar number of lymph nodes resected, hospitalization time, duration of surgery, postoperative drainage volume, air leak time and mortality [14]. But also in immunological terms, there are similar immune system activation profiles, decreasing IL-10 levels and total lymphocyte counts, and increasing serum levels of C-reactive protein, cortisol and glucose, among many other changes [15]. This may suggest that the response of the immune system will be similar between the two approaches. Since the late 1990s, it has been shown that the inflammatory pattern developed in serious diseases, including cancer, can influence prognosis and complications [16]. This is especially true in solid tumors. In these, marked lymphopenia and neutrophil are observed. In consequence, a high neutrophil-lymphocyte ratio may predict worse oncological and survival outcomes and more complications in certain cases. Therefore, new indices derived from blood components and analytical determinations, largely related to the inflammatory response, have been developed and are now widely accepted in this field. In particular, the platelet to lymphocyte ratio (PLR) and the lymphocyte to monocyte ratio (LMR) both have a very similar origin to the NLR. In recent years, a new indicator known as the systemic immune-inflammatory index (SII) has been described in relation to prognosis in hepatocarcinoma; this results from the ratio between the product of neutrophils and platelets and lymphocytes. This ratio expresses, in a combined form, the two previously mentioned markers. However, they have not shown adequate validation in lung cancer, even in the most rigorous meta-analyses, and vary according to different techniques and approaches [17, 18, 19, 20, 21, 22, 23]. Despite numerous efforts to clarify the relationship between immune response, inflammation levels and long-term oncologic outcomes, the evidence remains inconclusive. New drugs and therapies have been developed with the aim of modifying these phenotypes to alleviate different types of neoplasms by altering the proportions of various cell groups, enhancing their antitumor effects, and consequently modifying the derived ratios.