Hypothesis-driven research might be biased when researchers are obstinate in engulfing data fitting their hypothesis and do not get challenged with broader ideas. This is the singular story that happened to GLUT9 (SLC2A9). The glucose transporter (GLUT) family consists in 14 members classified as type I, II or III, based on sequence homology and on the ability to transport specific substrates. If Glut2 or Glut4 belongs to class I because of their capacity in transporting glucose, other GLUT members have less well characterized substrates and are spread between classes II and III. Glut9 has been cloned in silico by homology with other members of the GLUT family in 2000. Since then, it has been worked out as a poorly efficient glucose transporter of unknown function. In 2007 and 2008, several genome-wide association studies (GWAS) have documented a strong association between plasma uric acid levels and the GLUT9 gene and have revolutionized the way we looked at Glut9 and our approach to uric acid homeostasis. Subsequently, Glut9 has been shown to be a urate transporter, most probably a uniporter. It is involved in uric acid homeostasis, as illustrated by loss-of-function mutations found in humans that lead to familial hypouricemia. Moreover, Dalmatian dogs carrying Glut9 loss-of-function mutations and mice invalidated for Glut9 were found to express high level of uric acid in plasma and urine. In total, Glut9 has been shown to be essential for uric acid homeostasis. Geneticists have been instrumental in identifying the real function of Glut9, by using the powerful, hypothesis-free GWAS approach.