While the precise pathogenesis of HFSR is unknown, it is believed that the inhibition of RTKs, such as vascular endothelial growth factor receptors (VEGFR), particularly when combined with the inhibition of other endothelial RTKs, such as platelet-derived growth factor receptor (PDGFR), triggers the desquamation and hyperkeratosis observed in HFSR [1]. The gene discussed is KDR; the disease is Hyperkeratosis.