Epithelial–mesenchymal transition phenotype was envisioned as a pivotal pathological process, and its key biomarker SNAI1-mediated downstream signaling was adversely associated with the tumor-inhibition function of TRIM50 in breast cancer cells.33 Snail family members are EMT-activating transcriptional factor that directly bind to the proximal CDH1 promoter to inhibit E-cadherin and reshape the intercellular adhesion34; It also reconstructs epithelial polarized molecules and blocks the formation of basement membrane to build a predominantly invasive-inclined tumor microenvironment.35 This evidence concerns the gene TRIM50 and breast carcinoma.