Along similar lines, patients with bi-allelic SNX14 mutations share both clinical and pathological features of lysosomal storage (such as enlarged lysosomes) and autophagic (such as reduced autophagic flux) disorders, suggesting that deficits in both autophagy and lysosomal function may contribute to certain features of the clinical phenotype in SNX14-related ataxia such as prominent cerebellar involvement and Purkinje cell loss [107]. Here, SNX14 is linked to cerebellar ataxia.