At the pharmacological level, researchers are exploring (1): direct depletion of pro-tumor CAF subpopulations, such as using antibody-drug conjugates targeting FAP (2); inhibition of key signaling pathways, such as employing TGF-β receptor inhibitors to block myCAF differentiation and subsequent matrix deposition (3); modulating their immune function, such as “rescuing” iCAFs from immunosuppression via CXCL12-CXCR4 axis inhibitors to enhance T-cell infiltration (13, 15). Here, CXCR4 is linked to neoplasm.