In addition, overexpression of WNT5A triggered a feed-forward loop to activate SMAD2, via RYK and the transforming growth factor β-receptor 1 (TGFβR1), resulting in limited expansion of basal TICs, hence providing another possible but not proven explanation for the tumor-suppressive effects of WNT5A in breast cancer [24]. This evidence concerns the gene WNT5A and neoplasm.