This is seen in the case of low-grade Ta tumors that often carry activating mutations in fibroblast growth factor receptor 3 (FGFR3) and Harvey rat sarcoma viral oncogene homolog (HRAS), leading to activation of receptor tyrosine kinase–RAS–MAPK signaling [2,3,4], whereas a high-grade Ta tumor more frequently involves homozygous deletion of p16^INK4a and shares a reduced frequency with the FGFR3 mutation [5]. This evidence concerns the gene FGFR3 and Takayasu arteritis.