Most studies of biological mechanisms have suggested that the protective cellular effect of MHT on CRC is likely to be mediated through nuclear estrogen receptors (i.e., ERα, ERβ) and progesterone receptor, which may involve increasing DNA repair, selectively activating proapoptotic signaling, inhibiting expression of oncogenes, regulating cell cycle progression, changing the miRNA pool and DNA methylation [15]. The gene discussed is ESR1; the disease is colorectal carcinoma.