Early in NASH, KCs produce cytokines such as TNFα and IL1β, which worsen hepatic steatosis by inhibiting hepatic PPARα activity (63) and act as paracrine signals by increasing KC and hepatic stellate cell expression of Ccl2, which recruits inflammatory monocytes to the liver (64, 65). This evidence concerns the gene CCL2 and metabolic dysfunction-associated steatohepatitis.