Studies show that knockdown of SPCA1 results in disruption of Golgi morphology in HeLa cells,[48, 49, 50] and reduction of the amount of Ca2+ stored in the Golgi lumen.[49, 50, 51] The Golgi complex is tightly integrated into the urothelial cellular system, where it is crucial for the health of the blood–urine barrier, mainly through its association with uroplakins.[49] One can hypothesize that mutations of ATP2C1 may also result in a disruption of Golgi morphology in urothelial tissue, impairing the formation of the blood‐urine barrier, a hallmark of IC/BPS.[52]. This evidence concerns the gene ATP2C1 and Bartsocas-Papas syndrome 1.