These interactions underscore the complex network of protein interactions potentially involved in the pathophysiology of PWS, including other relevant proteins such as Ubiquitin-protein ligase E3A (UBE3A), Gamma-aminobutyric acid receptor subunit beta-3 and gamma-3 (GABRB3 and G3), the putative phospholipid-transporting ATPase VA (ATP10A), Gamma-tubulin complex component 5 (TUBGCP5), P protein (OCA2), and the magnesium transporters NIPA1 and 2 (Figure 3). This evidence concerns the gene TUBGCP5 and Prader-Willi syndrome.