In 1994, Shiang [3] found that ACH has mutations in the transmembrane domain of the fibroblast growth factor receptor 3 (FGFR3) [3] and more than 98% of ACH cases carried the base conversion that changes G to A at position 1138 of cDNA in exon 10 of FGFR3 gene, which changes the amino acid at position 380 of the FGFR3 from glycine to arginine. The gene discussed is FGFR3; the disease is achondroplasia.