Many oncogenic drivers of mCRPC, such as AR and MYC, were within peaks of amplification across the cohort, while tumor suppressors such as PTEN, TP53, and KMT2C were found within deletion peaks (Supplemental Figure 1C and Supplemental Table 1, E and F), consistent with prior reports (10, 13, 15, 36). This evidence concerns the gene PTEN and neoplasm.