Lysosomal dysfunction has also been seen as the basis of NCLs, whereupon research by Henderson et al. detected other lysosomal enzyme-associated proteins, including TPP1/CLN2, ATP6V1A, and LC3B II; they found no change in these proteins in the brains of patients with ANCL (Henderson et al., 2016). Here, TPP1 is linked to adult neuronal ceroid lipofuscinosis.