Overall, our above data indicated that KDM1A deletion was unable to induce endogenous DNA damage, which can activate cGAS-STING signaling in TME [34], we thus conclude that KDM1A inhibits STING-associated anti-tumor immunity in sTILs to drive ESCC tumorigenesis by blocking NF-κB-dependent proinflammatory genes directly through RAD51, as graphically summarized in Fig. 6G. The gene discussed is STING1; the disease is neoplasm.