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). The gene discussed is CALCOCO2; the disease is amyotrophic lateral sclerosis.