We found that the combination therapy robustly slowed the tumor growth and increased the survival rate only in CT26-cGAS-WT tumor model, while cGAS-KO tumor-engrafted mice did not respond to the combination therapy (Fig. 7f, g, Supplementary Fig. 7n, o), supporting the notion that the therapeutic benefit of PRMT1 inhibition in the syngeneic tumor model was largely cGAS-dependent (Fig. 7h, Supplementary Fig. 7p). This evidence concerns the gene DDX53 and neoplasm.