Chen et al. (2016) have found that TRIM14 could block cGAS degradation through selective autophagy and therefore promote innate immune responses during viral infections. Specifically, upon the viral infections, TRIM14 could recruit USP14 to cut the lysine 48 (K48)-linked ubiquitin chains of cGAS at K414, causing inhibition of p62-mediated autophagic degradation of cGAS, therefore promoting the activation of type I interferon signaling to aid the elimination of the invading viruses (Chen et al., 2016). The gene discussed is TRIM14; the disease is viral infectious disease.