It has been suggested that tamoxifen possesses untapped anticancer potential as an ASAH1 inhibitor, independent of estrogen signaling.18 We specifically hypothesized that the hormone‐independent effect was due to inhibition of PGCC progeny and, in support, the current study demonstrates that tamoxifen blocked colony formation by PGCC in prostate cancer, melanoma, and glioblastoma cells (Figure 2). Here, ASAH1 is linked to prostate carcinoma.