Accordingly, subcutaneous injection of lung carcinoma and melanoma cells into S1PR2-deficient mice led to accelerated tumor growth, in part due to enhanced infiltration of CD11b+ myeloid cells, which stimulated new vessel formation through secretion of proangiogenic mediators such as vascular endothelial growth factor A (VEGF-A) [159]. The gene discussed is S1PR2; the disease is neoplasm.