Cancer remains a major global health challenge, and a key barrier to durable responses is the ability of tumors to evade immune detection and elimination. Although substantial progress has been made in delineating mechanisms of immune escape, effective strategies to counter them remain limited. Emerging evidence positions double-stranded RNA (dsRNA) as a central modulator of tumor–immune interactions, with ADAR1-mediated adenosine-to-inosine (A-to-I) editing functioning as an inhibitory checkpoint that dampens innate and adaptive anti-tumor responses. However, the precise molecular pathways by which dsRNA editing and its regulators reprogram immune surveillance—and the downstream consequences for the tumor microenvironment—remain incompletely defined. In this talk, I will present recent findings that elucidate how dsRNA sensing and A-to-I editing intersect to suppress immunogenic signaling and influence the behavior of surrounding stromal and immune cells.