Moreover, we outline a therapeutic paradigm termed "proteostatic stress creation." This framework encompasses a spectrum of strategies, from precision protein-protein interaction inhibitors to state-selective degraders of DCAF12 or its ubiquitinated chaperonin subunits. These approaches can potentially disrupt the DCAF12-TRiC/CCT axis, thereby undermining the proteostatic resilience that sustains advanced cancers. This evidence concerns the gene DCAF12 and cancer.