Moreover, since IBI319 is a strong PD-1 binder (1137 times higher affinity for PD1 than for CD137), this design may localise most IBI319 molecules to microenvironments rich in PD-1-expressing T and NK cells, such as tumours and the TDLNs, and minimise systematic circulation, which may help limit off-target side effects. This evidence concerns the gene TNFRSF9 and neoplasm.