We also show that UDCA, an FDA approved drug linked to FTD/ALS therapy but whose mechanism of action is unclear [19, 59], stimulates VAPB-PTPIP51 binding and corrects TDP43 linked damage to the VAPB-PTPIP51 interaction and IP3 receptor delivery of Ca2+ to mitochondria. The gene discussed is ITPR1; the disease is amyotrophic lateral sclerosis.