These data show that, among livers with steatosis, a predisposition to form Ld-MaS, rather than Sd-MaS, is independently associated with: (a) the M variant of PNPLA3, a sign of abnormal lipolysis; (b) the administration of noradrenaline, and therefore poor blood perfusion of the liver; (c) a low hepatic expression of INSIG1 and NPC1L1, indicating sensing of a high intracellular cholesterol content and reduced activation of the cholesterol reabsorption pathway from bile; and (d) a high rate of HSC activation, a sign of predisposition to fibrogenesis. Here, PNPLA3 is linked to steatosis.