Thus, in order to effectively evaluate the therapeutic potential of targeting the ATG16L1-binding pocket in ATG5, further investigation into the potential ATG5-independent forms of autophagy; the nonautophagic functions of ATG5, ATG12, and ATG16L1; and the impact of ATG5 inactivation on tumor progression in different tissues and genetic backgrounds will be required. Here, ATG12 is linked to neoplasm.