Chloride mobilization appears to control CaMK-II and c-Src activities in breast adenocarcinoma cells, as chemically inhibiting or knocking down the chloride-channel ANO1 (anoctamin-1) with a shRNA (short hairpin RNA), reduced both epidermal growth factor receptor (EGFR) and CaMK-II activation, inducing afterwards a decrease of Akt/c-Src/MAPK (mitogen-activated protein kinase) activation, both in vitro cultured cells and in vivo using xenographted tumor cells, inhibiting therefore cancer progression, and underscoring the tumor promoting role of these pathways [87]. This evidence concerns the gene CAMK2G and neoplasm.