While our data do not support a universally pro-oncogenic role for the CC genotype in ECs, they instead suggest a genotype that could be associated with transcriptional quiescence and hormone receptor preservation, similar to what we find in BC subtypes, and the further mechanistic investigations of HSD3B1-permissive and -restrictive protein functions could contribute to novel insights in patients with EC. The gene discussed is HSD3B1; the disease is breast cancer.