Once the UPR is activated, tumor cells release pro-survival components including cytokines, growth factors, and other factors, which induce cancer cell growth and proliferation and suppressing anti-tumor immune response [14, 15], It is reported that when HCC mice were treated with the IRE1α-inhibitor, alleviation of tumor load and collagen accumulation were observed, which indicate that regulating ERS and UPR is an effective way to inhibit drug resistance to HCC. The gene discussed is ERN1; the disease is neoplasm.