FPGT (fucose-1-phosphate guanylyltransferase) catalyzes the conversion of GTP and L-fucose-1-phosphate to GDP-L-fucose 1, functioning as a salvage pathway enzyme that reutilizes L-fucose from glycoprotein and glycolipid turnover 1. This salvage pathway complements the de novo synthesis of GDP-L-fucose, which is essential for fucosylation of mammalian glycoproteins and glycolipids 2. Disease relevance: FPGT variants have been identified through genome-wide association studies as potentially influencing susceptibility to sickle cell disease nephropathy (SCDN), with FPGT-TNNI3K/TNNI3K loci showing significant association with decreased estimated glomerular filtration rate in adult SCD patients 345. Additionally, FPGT variants have been associated with chr1 pain and major depressive disorder in pleiotropy studies 6, and candidate gene analysis identified Fpgt as a likely contributor to viral myocarditis susceptibility 7. Clinical significance: These associations suggest FPGT may play a role in complex disease pathophysiology, though functional mechanisms remain unclear. The consistent identification of FPGT across multiple genome-wide association studies indicates potential value for genetic risk stratification, particularly in SCD populations at risk for renal complications.