Importantly, downregulating ALG3-induced under-glycosylation disrupts the binding capacity of TGFBR2 with TGFBR1, further attenuating phosphorylation of smad2 and inactivation of TGF-β signaling, which ultimately inhibits cancer cells stem-like traits and increased radiosensitivity in breast cancer cells. This evidence concerns the gene ALG3 and breast carcinoma.