Indeed, the presence of DSBs (likely to be higher in HRD tumors) has been found to upregulate PD-L1 expression in cancer cells, in a process that requires ATM/ATR/Chk1 kinases and is driven by STAT1 and STAT3 signaling, providing a potential explanation for the elevated PD-L1 seen in HRD tumors [117]. The gene discussed is CHEK1; the disease is cancer.