Notably, ATG16L2, as a paralog of ATG16L1, which N-terminal region also binds to the ATG5-ATG12 complex like ATG16L1, but is not recruited to the autophagosome membrane, possibly acting as a potential competitive ATG16L1 inhibitor to inhibit autophagy; in CRC, its overexpression inhibits tumor proliferation in vitro and in vivo, and is associated with usually a long survival rate (28). Here, ATG16L1 is linked to neoplasm.