We observed that the expression of a potent angiogenic factor, VEGF, in alkali-injured cornea was enhanced to a larger extent when the mice were treated with SDF-1α, consistent with the previous report that the CXCR4/SDF-1α axis can induce Akt phosphorylation and eventually augment VEGF expression at both the mRNA and protein levels, thereby promoting VEGF-mediated tumor angiogenesis [40]. The gene discussed is AKT1; the disease is neoplasm.