In a related manner, we speculate that the ALS-mutant p62 is neomorphic and can more readily interact with LC3C or GABARAPL2 in cellulo (as other hATG8 interactions are less efficient), potentially acting as a competitive inhibitor to the “normal” functions of LC3C and GABARAPL2, for example, given that LC3C selectively interacts with NDP52 or GABARAPL2 with UBA5 (37, 38). Here, MAP1LC3C is linked to amyotrophic lateral sclerosis.