Wild-type and four different FTD/ALS mutants of TDP43 including the two used in this study have been shown to disrupt the VAPB-PTPIP51 interaction and linked functions in neuronal cells and transgenic mice using quantitative assays, and expression of VAPB and PTPIP51 has been shown to stimulate ER-mitochondria signaling [47]. This evidence concerns the gene VAPB and amyotrophic lateral sclerosis.