Taken together, these data suggest that blockade of two non-redundant immune checkpoint pathways (PD-L1 and CTLA-4) may accelerate the immune infiltration into pancreatic islets, and we hypothesize that blockade of PD-L1 is a key factor for the development of ICI-induced IDDM in predisposed individuals. Here, CD274 is linked to type 1 diabetes mellitus.