There are a number of naturally occurring CLN6 animal models used in therapeutic development, including the Cln6nclf mouse model that contains a similar point mutation as found in human patients and develops the classical pathophysiological hallmarks of Batten disease, such as intracellular inclusion, retinal degeneration, hind-limb paralysis, and premature death [11–13]. The gene discussed is CLN6; the disease is juvenile neuronal ceroid lipofuscinosis.