To determine whether blockade of all 3 pathways (LAIR-1, PD-L1, and TGF-β) would be required to achieve optimal antitumor efficacy, bintrafusp alfa, anti–PD-L1, and a mutant version of bintrafusp alfa (designated as TGF-β trap control), which has no binding to PD-L1 while still sequestering TGF-β, were utilized as monotherapy or in combination with NC410 to comparatively treat MC38 tumor–bearing mice. The gene discussed is LAIR1; the disease is neoplasm.