These hits activate inflammatory cascades and pro-inflammatory cytokines, including interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), and IL-6, which contribute to NAFLD pathogenesis and cause subsequent progression to fibrogenesis (Cortez-Pinto et al., 2006), eventually leading to an increase in the prevalence of NAFLD/NASH. This evidence concerns the gene IL1B and metabolic dysfunction-associated steatotic liver disease.