The solid evidence supporting the induction of autophagy in favor of ZIKV infection comes from the colocalization of cytosolic microtubule-associated molecule LC3 and the ZIKV E protein in the infected fibroblasts as well as the observation of elevated ZIKV replication when stimulates the autophagosome formation, which suggests ZIKV utilizes the autophagic vesicles as viral replication site [25]. This evidence concerns the gene MAP1LC3A and Zika virus infectious disease.