The mitochondrial protein CPT1A recruits the endoplasmic reticulum-localized ZDHHC4 to catalyze MAVS C79 palmitoylation, which increases MAVS stability and activation by inhibiting K48-linked ubiquitination but facilitating K63-linked ubiquitination, thereby enhancing the IFN-I response and enhancing control of viral infection [91]. This evidence concerns the gene MAVS and viral infectious disease.