The development of MAFLD in individuals with high CHR may be mediated through two key pathophysiological mechanisms: on the one hand, inflammation of the adipose tissue (e.g., the release of the proinflammatory cytokine tumor necrosis factor) promotes insulin resistance, thereby releasing large amounts of free fatty acids and causing hepatic steatosis [26]. The gene discussed is INS; the disease is Hepatic steatosis.