Interactions between obesity, ERα, p53 and EMT are highly plausible because: 1) obesity increases mammary aromatase expression and serum estradiol levels [25]; 2) obesity upregulates EMT in MMTV-Wnt-1 basal-like mammary tumors and Met-1 luminal-type mammary tumors expressing wild-type p53 [26], [27]; 3) the loss of p53 in human breast cancer cells results in EMT-associated stem cell-like features [28]; and 4) p53 suppresses cell invasion by initiating the degradation of slug and increasing E-cadherin expression [29], and slug, in turn, can repress p53-mediated apoptosis [30]. The gene discussed is SNAI2; the disease is obesity due to melanocortin 4 receptor deficiency.