Taken together, our results (1) support further development of FAP-RLT for the treatment of tumors with high FAP expression, (2) suggest that FAP-targeted RLT could be leveraged to re-sensitize immunosuppressed tumors for ICB, and (3) imply that the pharmacokinetic profile of FAPI-46 might be insufficient to achieve profound anti-tumor efficacy, which is why currently new compounds are being tested in clinical trials [31–34]. The gene discussed is FAP; the disease is neoplasm.