PIGT (phosphatidylinositol glycan anchor biosynthesis class T) is a subunit of the glycosylphosphatidylinositol transamidase (GPI-T) complex located in the endoplasmic reticulum membrane 1. The complex catalyzes attachment of GPI anchors to proteins, a critical post-translational modification that tethers numerous proteins to cell surfaces 1. PIGT plays a crucial role in GPI-T complex assembly and directly binds GPI anchors 1. Beyond its canonical function, PIGT promotes cell growth and glycolysis in bladder cancer by modulating GLUT1 glycosylation and membrane trafficking through m6A mRNA modification 2. Pathogenic PIGT variants cause Multiple Congenital Anomalies-Hypotonia-Seizures Syndrome 3 (MCAHS3), characterized by dysmorphic features, severe hypotonia, developmental delay, and intractable seizures including epileptic apnea 345. Biallelic mutations result in impaired GPI-anchored protein synthesis, evidenced by reduced expression of GPI-anchored proteins like CD59 and CD16 45. PIGT mutations also cause Paroxysmal Nocturnal Hemoglobinuria 2 (PNH2), a distinct clinical entity from PIGA-driven PNH with autoinflammatory manifestations 6. PIGT defects are additionally associated with congenital cardiac defects as part of glycosylation-linked metabolic disease 7.