Assuming from the studies of Le Cornet and coworkers that there is no correlation between circulating 26‐HC and breast cancer risk [119, 120], and in direct contrast to the suggestion of Nelson to inhibit CYP27A1 [117], enhancing CYP27A1 expression or activity should drive cholestane‐3β,5α,6β‐triol into the bile acid biosynthesis pathway and away from metabolism by HSD11B2 to oncosterone. The gene discussed is CYP27A1; the disease is breast cancer.