Disease progression beyond NAFL (i.e., NASH, fibrosis, etc.)has been shown to be promoted by the generation of hepatic reactive oxygen species (ROS), macrophage activation, transforming growth factor beta 1 (TGF-β1)-mediated collagen deposition, imbalance between Th17 and regulatory T cells (Treg), and metabolic activation of intrahepatic CD8+ T cells and natural killer T cells (NK-T) (6, 7). Here, CD8A is linked to metabolic dysfunction-associated steatohepatitis.