While loss of KLF4 function induces EMT-like morphological changes, forced expression of KLF4 in invasive breast cancer cells induces epithelial differentiation by directly repressing the expression of Snail1, a potent repressor of E-cadherin gene expression, and directly binding to the E-cadherin promoter and upregulating E-cadherin expression [10]. This evidence concerns the gene KLF4 and breast cancer.