Since elevated CCL2 initiates inflammatory reaction by increasing production of nitric oxide and other inflammatory chemokines from unregulated monocytes/macrophages [26] and VEGF-A is known to recruit leukocytes at the site of brain injury by increasing vascular permeability [27], it is possible that the high VEGF-A and CCL2 in our ALS patients may exert limited inflammatory responses associated with neuroprotection [28]. The gene discussed is VEGFA; the disease is amyotrophic lateral sclerosis.