Additionally, in the co-culture of murine hepatocytes and HSCs, lentiviral overexpression of CXCL16 increased lipid accumulation and mitochondrial stress in hepatocytes and induced the activation and proliferation of HSCs [55], suggesting that the CXCL16-CXCR6 axis mediates the crosstalk between hepatocytes and HSCs in NAFLD development. The gene discussed is CXCL16; the disease is metabolic dysfunction-associated steatotic liver disease.