Interestingly, while CLN6 has not been found to colocalize with any lysosomal markers, loss of CLN6 ultimately leads to classic Batten disease pathology, including accumulation of aggregates in the lysosome (autofluorescent storage material, mitochondrial ATP synthase subunit C (SubunitC)), enhanced glial activation, neuron loss, motor, visual, and memory/learning decline, and ultimately early death. The gene discussed is CLN6; the disease is juvenile neuronal ceroid lipofuscinosis.