Our findings are consistent with previous studies reporting that ESRP1 causes phenotypic switching via regulation of epithelial or mesenchymal isoforms of CD44 or ENAH in mouse18 or human breast cancer cells24, 25 and human bronchial epithelial cells.9 Importantly, levels of ENAH11a isoforms are positively correlated with a high proliferation index and E-cadherin expression in human primary breast tumor tissues,25 in agreement with our data showing that ectopic ESRP1 expression upregulates both CDH1 and ENAH11a expression. This evidence concerns the gene CDH1 and breast neoplasm.