This notion was strongly reinforced by our recent manuscript, that pinpoints that hepatic MBOAT7 down-regulation is a maladaptive response to hyperinsulinemia and that its hampered enzymatic activity forces hepatic fat storage in patients, in in vivo models representative of NAFLD and in MBOAT7 silenced HepG2 hepatoma cells (also referred to as MBOAT7−/−) [109,132]. This evidence concerns the gene MBOAT7 and hyperinsulinism.