Our further investigation demonstrates that miR-30b-5p and miR-30c-5p, which are upregulated after eIF2α phosphorylation has increased, target eIF2α, lead to suppression of the p-eIF2α-ATF4-CHOP pro-apoptotic pathway, and thereby promote cell proliferation and confer resistance to apoptosis in the cancer cells both under basal culture condition and during proteasome inhibition, unraveling a new miRs-based mechanism for suppressing general protein synthesis and improving cell survival in the UPR. This evidence concerns the gene DDIT3 and cancer.