Given the TGFβ signaling pathway alterations found in human endometrial tumors, we generated mice with epithelial-specific inactivation of Smad225 and Smad315 using Ltf-cre26 (“Smad2/3 cKO” mice) to investigate the in vivo roles of SMAD2 and SMAD3 signaling in the luminal uterine epithelium, (Fig. 1a). This evidence concerns the gene SMAD2 and endometrium neoplasm.