Researchers at Northwestern reported a new class of protein‑like polymers—HYDRACs—that recruit cellular degradation machinery to eliminate traditionally 'undruggable' oncogenic drivers such as MYC and KRAS. In cell culture, HYDRACs selectively reduced target protein levels and triggered cancer cell death; tumor accumulation and growth inhibition were observed in mouse models. The HYDRAC approach fuses multivalent target‑recognition motifs with degron elements on a polymer scaffold, bringing targets into proximity with the ubiquitin‑proteasome or autophagy systems. Unlike small‑molecule inhibitors that require defined binding pockets, this proteomimetic strategy can engage disordered proteins and expand the druggable proteome. If translatable, HYDRACs could open new avenues for targeting drivers long considered intractable, but the path to clinical application will hinge on delivery, specificity, immunogenicity, and in vivo durability.