However, certain cancer cell autonomous mechanisms regulating proteostasis can either subvert danger signaling pathways (like the PERK-eiF2α axis [66]), cause retention of DAMPs thereby impairing the proficient dialogue between dying cancer cells and the immune system or secrete mutate forms of DAMPs (like mutant CRT) which supposed to act as a decoy for DCs in the wild-type [67]. This evidence concerns the gene CALR and cancer.