Expression of both wild-type and familial FTD/ALS mutants of TDP43 have been shown to disrupt the VAPB-PTPIP51 interaction, reduce ER-mitochondria contacts, inhibit IP3 receptor delivery of Ca2+ to mitochondria and to activate GSK3β to similar extents [47]. This evidence concerns the gene ITPR1 and amyotrophic lateral sclerosis.