On the one hand, it activates cGAS/STING to boost tumor immunogenicity, on the other hand, it induces the expression of immunosuppressive regulators, such as PD-L1 21 and Gal-9, to inhibit T cell activation and elicit T cell death, etc. Intriguingly, although we found that PD-L1 could also be upregulated in response to ATM inhibition, the extent of its alteration is minimal compared with that of Gal-9, suggesting that Gal-9, but not PD-L1, likely plays a predominant role in mediating the immunomodulation by ATMi. Here, CGAS is linked to neoplasm.