CD8A and steatosis: Differential activation of iNKT cells skewed from predominantly NKT17 (IL-17+ iNKT and IL-22+ iNKT) to NKT1/NKT2 (IFNγ+ iNKT, IL-4+ iNKT and IL-13+ iNKT) played a pathogenic role in mediating the progression from steatosis to fibrosis by promoting the infiltration of CD8+ T cells and macrophages and the activation of HSCs (106).