Importantly, in contrast to recent studies that proposed that DNASE1L3 suppresses tumor growth via cancer cell–autonomous mechanisms such as increasing apoptosis, modulating glycolysis, or decreasing migration using epithelial cancer cells with artificially overexpressed DNASE1L3 (33, 34), we demonstrate that Dnase1l3 deficiency in the tumor microenvironment rather than in tumor cells is sufficient to induce tumor growth and impair antitumor immunity. Here, DNASE1L3 is linked to cancer.