The absence of GPD accumulation in our zebrafish model for ATP13A2/CLN12 deficiency (35), also leading to neuronal lipofuscinosis (54, 55, 56), indicates that these compounds may be specific for certain types of NCLs, a hypothesis that will now need to be tested in different models and non-CLN3 Batten disease patients. This evidence concerns the gene ATP13A2 and juvenile neuronal ceroid lipofuscinosis.