Furthermore, a gradual increase in size occurred over 4 years, and there was negative immunostaining for GLUT-1, which is a downstream target of hypoxia-inducible factor 1 alpha.[26] There was also negative immunohistochemical reactivity for VEGF-A and IGF-2, which are sensitive markers for the diagnosis of infantile hemangioma.[27] These findings suggest that the tumor was not a residual anomaly of a congenital hemangioma but rather that it developed in adulthood. The gene discussed is HIF1A; the disease is congenital hemangioma.