In this context, a complex relationship among increased 18F-FDG uptake, tumor hypoxia, and neoangiogenesis has been observed: hypoxia-inducible factor-1 alpha (HIF-1a), which is upregulated under hypoxic state, is able to induce an up-regulation of GLUT-1 expression (so increasing the energetic supply of tumor cells) and may also induce the expression of the vascular-endothelial growth factor (VEGF), which promotes tumor cell survival and growth stimulating tumor neoangiogenesis (so increasing the tumor blood supply). Here, HIF1A is linked to neoplasm.