In MCF7 human mammary adenocarcinoma cells, a delicate balance of Src activity was required for maintaining normal adherens junction integrity, since either blocking Src activity (via dominant negative Src constructs or pharmacological inhibition using PP2) or overactivation of Src (by expression of the constitutively active mutant Y530F Src) induced a marked junctional disruption [47]. This evidence concerns the gene SRC and breast adenocarcinoma.