While it is possible that there is a specific function for ATM in mediating ATR/CHK1 signaling leading to PD-L1 induction, our study demonstrates from a broad perspective, including potent ATM inhibitors, multiple cell lines, and functional studies of CD8+ T cells that ATM inhibition enhances PD-L1 expression in pancreatic cancer treated with radiation, likely surpassing any potential negative regulation mediated by ATM/ATR/CHK1 signaling. The gene discussed is CHEK1; the disease is pancreatic neoplasm.