A subset of these cross-species modifier genes interact, directly or indirectly, with previously described neurological or neuromuscular disease proteins suggesting common neurodegenerative pathways may be at work (i.e. ATF6 with VAPB/ALS8 or GPRK2 and SMN1 with FMRP) [75]–[77]. This evidence concerns the gene SMN1 and glycogen storage disease VI.