This model posits that the disease arises from the synergistic effects of various concurrent factors, including metabolic disturbances, genetic predispositions, and environmental influences such as insulin resistance, adipokine dysregulation (such as reduced adiponectin and elevated pro-inflammatory cytokines like tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6)), and gut microbiota alterations (dysbiosis), which all contribute to the development of MASLD and its progression to MASH [6]. This evidence concerns the gene IL6 and metabolic dysfunction-associated steatotic liver disease.