A previous study associated breast cancer risk with defects in methionine metabolism and a methionine-dependence phenotype in BRCA1/2 mutation carriers.39 These intriguing links between BRCA2 mutation status with metabolic dependency warrant further preclinical study to establish a potential rational combination therapy of poly(ADP)-ribose polymerase inhibitors and MAT2A or PRMT5 inhibitors in MTAP-loss GI cancers. The gene discussed is MAT2A; the disease is breast carcinoma.