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). Here, EPM2A is linked to progressive myoclonus epilepsy.