In addition, some studies have shown that the deletion of ADAR1 is highly sensitive to tumor immunotherapy, overcoming the resistance of immune checkpoint blockade (ICB), and the deletion of ADAR1 can reduce the A to I editing of endogenous dsRNA, triggering MDA5 and PKR interferon-dependent anti-tumor response, subsequent tumor growth inhibition and pro-inflammation (62). Here, EIF2AK2 is linked to neoplasm.