Following the highlighting of the pivotal role of DGAT2 in hepatocytes where it is suggested to act as the link between glycemia, steatosis, and dyslipidemia15, 38 and, soon afterwards, of the unsuccessful phase 1 trials of DGAT1 inhibitors in humans,39 the interest in pharmacological manipulation of DGAT activities has shifted from DGAT140 to DGAT2.41 The gene discussed is DGAT2; the disease is steatosis.