STK17A was first identified as a proapoptotic human kinase,32 and rodents were shown to lack a homologous gene.33 Some reports indicated that STK17A induction in cancer cells enhances cell sensitivity to anticancer agents.34 BMP2K was first isolated from prechondroblastic cells treated with BMP-2 and was shown to negatively regulate osteoblast differentiation.35 On the basis of these data, it seems unlikely that development of the prevalent adverse reactions associated with sunitinib can be explained by STK17A or BMP2K inhibition. The gene discussed is BMP2; the disease is cancer.