Although acquisition of PTEN genetic alterations in response to the p110α inhibitor alpelisib (BYL719) have been shown to drive resistance in metastatic breast cancer patients [85], indicating that similar mechanisms of resistance may emerge in PTEN-deficient prostate cancer, p110α inhibition may still prove to be efficacious against prostate cancers that are both PTEN-deficient and carrying an activating PIK3CA mutation. Here, PIK3CA is linked to prostate carcinoma.