TGFB1 and neoplasm: In fact, several recent studies suggest that alterations in ECM proteins, fibrillar collagens, CAFs, and increased expression of TGF-β all contribute to fibrosis and play key roles in resistance to immunotherapy by creating a physical barrier inhibiting T cell infiltration (immune exclusion) that is crucial for anti-tumor immunity and concomitant clinical responses to current checkpoint inhibitors (49–61).