TGF‐β1 highly expression within the cancer microenvironment restrains immune surveillance therefore promotes the cancer invasion and enhances anti‐cancer immune responses resistance.40 Previous studies showed that TGF‐β1 stimulation caused phosphorylation of Smad2 and Smad3 and in turn their accumulation in the nucleus to promote Snail transcription,41 which in turn regulates EMT by effects on epithelial cell markers such as E‐cad.42 This evidence concerns the gene SNAI1 and cancer.