Thus, multiple components (hepatic lipid accumulation, oxidative stress, ER/mitochondrial stress, hepatocyte cell death, hepatocyte-released DAMPs/extracellular vesicles, Kupffer cell activation, inflammatory cell recruiting, HSC activation, insulin resistance, adipose tissue inflammation, and microbiota dysbiosis) are attractive therapeutic targets to treat NAFLD/NASH. This evidence concerns the gene INS and metabolic dysfunction-associated steatotic liver disease.