SLC5A2 and Renal glucosuria: According to a report on 86 mutations in Slc5a2 that caused familial renal glucosuria in humans, the mutations are primarily missense (75.6%), frameshift (8.1%), splicing (5.8%), and nonsense (4.7%) mutations, and the most common mutation sites are exon 11 (18.6%), exon 8 (12.8%), and exon 4 (11.6%) [10].