found that acute liver injury induced by IFN-α-mediated virus infection could be alleviated by inhibiting GRP78 through a mechanism that involves IFN-α induction of ER stress-related cell death by reducing the unfolded protein response (UPR), with GRP78 promoting high UPR expression and reducing IFN-α-mediated liver injury in mice (74). The gene discussed is IFNA1; the disease is viral infectious disease.