CTLA4 and injury: This hypothesis has shown promise in developing valid animal models of IDILI as demonstrated by a halothane induced liver injury mouse model developed by depleting myeloid derived suppressor cells (MDSCs), as well as an amodiaquine-, isoniazid-and nevirapine-induced liver injury mouse model developed by impairing immune tolerance by blocking PD-1 and CTLA-4, two immune checkpoint inhibitors.