As mentioned earlier, the key character of NASH was the loss of the liver’s tolerance to the microenvironment, which turned the liver into a pro-inflammatory immune phenotype and subsequently released pro-inflammatory cytokines to induce DCs maturation, and finally increased adaptive immune responses by CD4+/CD8+ T cells activation and infiltration (62, 63). Here, CD4 is linked to metabolic dysfunction-associated steatohepatitis.