Our syngenic MC38 tumor experiments, performed in immunocompetent Dnase1l3-KO mice, further demonstrated that deletion of Dnase1l3 in the recipient microenvironment rather than in the s.c. grafted epithelial tumor cells, promotes tumor growth, decreases activation of cDC1 and cDC2, and diminishes the abundance and function of cytotoxic T cells in tumors (Figures 5 and 6 and Supplemental Figure 6). Here, DNASE1L3 is linked to neoplasm.