After administration into a tumor-bearing mouse model, FBN@M specifically targets the tumor region following innate inflammation-directed chemotaxis of MΦM and NaHCO3 in response to acidic TME since the permeability of H+ inside generates CO2 to break up MΦM, leading to the release of BMS-202 and blocking the PD-1/PD-L1 pathway 52. Here, PDCD1 is linked to neoplasm.