This concept was recently reinforced by Meroni and colleagues who elegantly demonstrated that hepatic MBOAT7 down-regulation is a maladaptive response to hyperinsulinemia and that the impaired enzymatic activity forces hepatic fat storage in patients, in in vivo models, representative of NAFLD and in MBOAT7 silenced HepG2 cells [43]. This evidence concerns the gene MBOAT7 and metabolic dysfunction-associated steatotic liver disease.