The pathophysiology of NAFLD/MAFLD has evolved from a “first strike” characterized by increased hepatic fat to a “second strike” consisting of adipokines, inflammatory cytokines, oxidative stress, and mitochondrial dysfunction; and the “multiple strikes” hypothesis consisting of insulin resistance, inflammation, lipotoxicity, cytokine imbalance, innate immune activation and microbiota disorders in the background of genetic and environmental factors (60–62). Here, INS is linked to metabolic dysfunction-associated steatotic liver disease.