Sang et al. demonstrated that by increasing tumor cytosolic calcium concentrations, hypoxia could activate the PNCK-CamK-A-NF-κB axis and its downstream target genes, including glucose transporter 3 (GLUT3), interleukin 6 (IL-6), interleukin 8 (IL-8), and vascular endothelial growth factor (VEGF). The gene discussed is NFKB1; the disease is neoplasm.