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). The gene discussed is ASAH1; the disease is prostate cancer.