Disabling SMARCA2 is synthetic lethal with the loss of its paralog SMARCA4, which is frequently mutated in multiple solid tumours, including nonsmall cell lung cancer, bladder cancer and small cell carcinoma of the ovary. Accordingly, PRT3789—a SMARCA2‐selective degrader—was recently evaluated in a Phase 1 trial, with responses observed in some SMARCA4‐mutant tumours, thereby demonstrating the proof‐of‐concept utility of this approach [23]. This evidence concerns the gene SMARCA4 and neoplasm.