Recently, Clec16A, a protein associated with development of multiple sclerosis, has been shown to be required for autolysosome function in mouse models: in the absence of Clec16A both neuronal endocytosis and autophagy initiation are unperturbed, however, autolysosomes accumulate due to lacking regeneration of protolysosomes [312]. Here, CLEC16A is linked to multiple sclerosis.