Conversely, as expected by the presence of a mutant p53 in BC-PAP cells [30], treatment with EGF in these cells resulted in an opposite regulation of the above mentioned genes, including upregulation of EpCam and Fibronectin, and down-regulation of Caldesmon and RhoE, with the consequent activation of the EMT and cell migration programs (which are not opposed by a functional p53). This evidence concerns the gene EPCAM and breast cancer.