Oregon Health & Science University (OHSU) researchers reported that the cancer-driving MYC protein directly contributes to DNA repair mechanisms used by tumor cells under genotoxic stress. The study reframes MYC’s role beyond transcriptional activation, positioning it as a participant in the DNA damage response. The findings suggest cancer cells leverage MYC-linked repair to survive treatments that induce DNA lesions, potentially expanding the rationale for combination strategies pairing MYC pathway modulation with genotoxic therapies. For drug developers, the report highlights a targetable dependency that may help explain resistance patterns in tumors exposed to chemotherapy or radiation-related damage.