El Hiani et al. (2009) demonstrated that the proliferative effect of CaSR on breast cancer MCF-7 cells was mediated by the upregulation of TRPC1 protein and the activation of the ERK1/2 pathway. Nevertheless, continuously activated ERK1/2 by overexpressing CaSR facilitated apoptosis and reduced cell viability in neuroblastoma cell lines (Casalà et al., 2013). This evidence concerns the gene CASR and breast carcinoma.