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Inactivating alterations in SPOP frequently occur in prostate cancer and promote increased dependency on androgen receptor (AR)‐mediated oncogenic signaling. The presence of SPOP mutation (SPOP‐mutant [SPOP‐mut]) may therefore impact therapeutic outcomes with AR‐directed therapies and docetaxel in metastatic castration‐resistant (mCRPC). Furthermore, inactivating mutations in SPOP are associated with better response to ARSI treatment in mCRPC overall. Additional analysis with a larger cohort is needed to evaluate the association of SPOP status and outcomes with docetaxel. Nevertheless, race-associated clinical outcomes and molecular features were observed, suggesting the benefit of biomarker‐directed therapy selection for individualized patient subsets in guiding treatment decisions for mCRPC patients.
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