More recently, however, a couple of studies have demonstrated that the tumor-suppressing effect of Dac can be attributed to an activated innate immune response, in which an increase of endogenous dsRNA stimulates retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated protein 5 (MDA5) and can then trigger mitochondrial antiviral signaling protein (MAVS)/interferon regulatory factor 3 (IRF3) pathway, ultimately leading to cell death [16,17]. Here, MAVS is linked to neoplasm.