In the past few years, SNAI1 has emerged as one of the important classical EMT transcription factors in cancer research.20 SNAI1 repression of E-cadherin involves the direct recruitment of a repressor complex formed by the corepressors SIN3A and HDAC1/2.21 Some histone modifiers such as the methyltransferases G9a22 and Suv39H123 are associated with SNAI1 activity in human breast cancer. This evidence concerns the gene SNAI1 and breast cancer.