In a recent study published in Nature, Laqtom et al. reported a novel function of CLN3 in the clearance of glycerophospholipid from lysosomes via lysosomal efflux of glycerophosphodiesters (GPDs), not only establishing a deeper mechanistic understanding of Batten disease, but also suggesting both the diagnostic and therapeutic potential of CLN3-GPDs in this type of neurodegenerative LSD. The gene discussed is CLN3; the disease is juvenile neuronal ceroid lipofuscinosis.