Proinflammatory cytokines (tumor necrosis factor alpha (TNFα) and interleukin 6 (IL6)) play an important role in the etiology and pathogenesis of non-alcoholic fatty liver disease (NAFLD), since they can promote inflammation and regulate apoptosis and necrosis of liver cells, induce fibrosis. Cytokines perform their functions through interaction with membrane-bound and soluble receptors on the cell surface, and the soluble forms of receptors may act as antagonists or as enhancers of their biological effects. Differences in the level of cytokines and soluble and membrane-bound cytokine receptors may be due to the presence of mutations in different regions of the corresponding genes. This may influence the formation of the signaling pathway that determines the fate of cells (i. e., survival, apoptosis or necrosis) and, accordingly, the development and progress of NAFLD, some forms of which, in particular steatohepatitis and cirrhosis, involve intensified hepatic cell death. However, the question of whether the polymorphism of TNF, IL6 genes and their receptors affects NAFLD development and progress currently remains largely uninvestigated. This paper presents current data from the literature investigating the relationship between TNF, IL6, TNFRSF1A, TNFRSF1B, IL6R gene polymorphism andthe development of non-alcoholic fatty liver disease.