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MTAP deletion and mutational activation of KRAS create therapeutic vulnerabilities for MTA-cooperative PRMT5 and mutant-selective KRAS inhibitors, respectively, providing the rationale for their combination therapy for MTAP-deleted, KRAS-mutant pancreatic cancer. See related article by Knoll et al., p. 3518.
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Drizyte‐Miller et al. (2025) studied this question.
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