Furthermore, silencing lipoprotein-associated phospholipase A2 (Lp-PLA2) in KCs and NAFLD model mice inhibited the activation of the JAK2/STAT3 signaling pathway, mitigated lipid accumulation, promoted autophagy, reduced production of inflammatory factors, and inhibited the progression of NAFLD (179). The gene discussed is STAT3; the disease is metabolic dysfunction-associated steatotic liver disease.