It cannot, therefore, be excluded that bi-directional cross-talk between integrin αvβ3 and ERα via ERK1/ERK2 activation in membrane-associated and/or cytosol localizations, which may result in the phosphorylation of nuclear tamoxifen-liganded ERα and its associated coactivators, might be part of the CCN1-driven endocrine resistant phenotype in breast cancer cells. This evidence concerns the gene MAPK3 and breast carcinoma.