In this work, treatment of NASH mice with IL-33 enhanced expression of Th2 cytokines (IL-4, IL-5 and IL-13) and M2 markers (Arg-1 and CD206), and reduced Th1 cytokines (IFN-γ) and M1 markers (IL-12p70 and TLR2), indicating that IL-33 promoted Th2 cytokine synthesis leading to the polarization of liver macrophages/Kupffer cells toward an M2 phenotype, and ultimately shifted the cytokine imbalance towards anti-inflammation, which might be beneficial for reversing hepatic steatosis. The gene discussed is IL5; the disease is metabolic dysfunction-associated steatohepatitis.