Assuming that metabolic adaptations are a hallmark of cancer cells [28] and the importance of ERRα/PGC-1 axis in controlling cellular adaptation to energy demand, it is not surprising that in breast cancer, the hyperactivation of ERRα, due to increased availability of CHOL leads to metabolic reprogramming aimed at promoting and maintaining energy-consuming processes such as cell proliferation and migration [29,30] and providing a mechanistic explanation for the increased breast cancer risk associated with high dietary CHOL [31]. This evidence concerns the gene ESRRA and cancer.