Myeloid-specific RORα-null mice are more susceptible to HFD-induced NASH due to decreased M2 polarization of Kupffer cells, decreasing interleukin 10 (IL-10) and increasing tumor necrosis factor alpha (TNFα) and interleukin 6 (IL-6) production, leading to lipid accumulation and hepatocytes apoptosis. This evidence concerns the gene IL10 and metabolic dysfunction-associated steatohepatitis.