Together, these results reveal a mutual regulatory mechanism involving canonical autophagy and CMA and highlight an important role for HSPA8 in viral release; that is, HSPA8 recruits ULK1 and induces its degradation via CMA during EV-A71 infection, thus decreasing autolysosome formation and increasing secretory autophagic release, which is in line with the mechanism by which EVs employ 3Cpro to cleave the SNARE complexes to prevent the fusion of autophagosome with lysosome (Corona et al., 2018; Mohamud et al., 2018). The gene discussed is ULK1; the disease is infection.