Moreover, in NAFLD and aging, increased visceral adipose tissue is associated with increased infiltration of M1 macrophages, which triggers adipose tissue IR and inflammation and leads to a disturbed adipokine profile (low adiponectin, an anti-inflammatory adipokine with beneficial effects in NAFLD; and high levels of pro-inflammatory adipokines such as leptin, IL-1β, IL-6 and tumor necrosis factor-α; TNF-α), which finally induces liver inflammation and hepatic IR, as previously stated [51]. The gene discussed is LEP; the disease is metabolic dysfunction-associated steatotic liver disease.