Although some exploratory results on LSEC-induced activation of CD4+ T cells in murine hepatic fibrosis have been previously described in a T CD8+ cell-specific activation centered study [37], here, we outlined that in the CCl4 model of experimental cirrhosis, LSECs were able to cooperate in the induction of effector Th17 subpopulations and to overcome the tolerogenic Treg differentiation profile in these animals, even at higher rates than hepatic DCs and HMs in this context, probably due to their immediate exposure to spontaneous bacterial translocation episodes. The gene discussed is CD8A; the disease is Cirrhosis.