When treated with metabolic stimuli (including acetate and extracellular ATP), CXCR6+ CD8+ T cells function as auto-aggressive cells in a way independent of MHC-class-I, which is induced by increased calcium influx and leads to the upregulation of FasL and apoptosis of hepatocytes thus promoting NASH (122–124). This evidence concerns the gene FASLG and metabolic dysfunction-associated steatohepatitis.