US28-expressing NIH-3T3 fibroblasts and U251 glioma cells have been shown to promote the transcriptional activity of HIF-1α under normoxic conditions via constitutive activation of Gαq by stimulating the calcium/calmodulin-dependent protein kinase type II (CaMKII) and the subsequent stimulation of Akt [29] (Figure 2). This evidence concerns the gene HIF1A and glioma.