CD274 and neoplasm: Furthermore, TGF-β could prompt the tumor immune escape and the resistance of immune therapy (47), which has been validated in the IMvigor210 cohort in which BC patients not responding to the therapeutic treatment of anti–PD-L1 agent (Atezolizumab) were highly correlated with the TGF-β signature in fibroblasts and commonly had fibroblast- and collagen-rich peritumoral stroma (48).