Mice having homozygous deletion in hypoxia response element (HRE) of VEGF-A promoter (VEGFδ/δ) were reported to develop symptoms like classical ALS [3] and conversely, intrathecal transplantation of stem cells overexpressing VEGF-A delays the onset and progression of ALS in superoxide dismutase-1 (SOD1) mutated transgenic mouse by downregulating proapoptotic proteins and activating phosphatidylinositol 3-kinase/protein kinase B (PI3-K/Akt) anti apoptotic pathway [4]. The gene discussed is VEGFD; the disease is amyotrophic lateral sclerosis.