In in vitro and in vivo models of pancreatic cancer, ATM inhibitors increased the expression of type I IFN and then activated immune signaling transduction, while the inhibition of ATM upregulated the expression of PD-L1 and also promoted the response of pancreatic tumors to anti-PD-L1 therapy, indicating the enhanced immunotherapy efficacy by ATM inhibitors and the strong potential of combinational therapy [160]. Here, CD274 is linked to familial pancreatic carcinoma.