Additionally, Wang et al. created an immune checkpoint ligand-engineered β cell to treat type 1 diabetes mellitus (TIDM) by suppressing islet-specific T cell function.236 It has been observed that β cells are deficient in PD-L1 (a co-inhibitory ligand for PD-1), CD86 (a co-inhibitory ligand for CTLA-4), and Gal-9 (a co-inhibitory ligand for TIM3), all of which linked to the development of T1DM.237–239 Based on this, the researchers employed DBCO dendrimers to attach PD-L1, CD86, and Gal-9 to N3-labeled β cells, creating PD-L1/CD86/Gal-9-modified β cells. This evidence concerns the gene HAVCR2 and type 1 diabetes mellitus.