ESR1 and breast cancer: Consistently, Lucki et al. (2011) have provided a mechanism to explain genistein’s ability to promote the proliferative response of MCF-7 cells via an estrogen-dependent ER-binding pathway, which predicts that genistein induces acid ceramidase (ASAH1) gene expression by activating a cell surface receptor-coupled G-protein (GRP30)-dependent pathway leading to the phosphorylation of ERK1/2 which in turn triggers the proliferative response of BC cells via an estrogen-dependent pathway.