Which proteins are the precise target(s) of malin remains unknown, but absence of malin’s function, like absence of laforin, leads to poorly branched and insoluble glycogen (polyglucosans), which accumulate in neuronal somatodendritic compartments into Lafora bodies (polyglucosan bodies), over time driving the neurodegeneration and progressive myoclonic epilepsy[28] (Fig 3). This evidence concerns the gene NHLRC1 and progressive myoclonus epilepsy.