Thus, our results in AUD patients with frontal deficits might suggest two things: (1) chronic alcohol abuse might lead to alterations in the concentrations of VEGFA that increase the permeability of the blood–brain barrier, leading to infiltration of immune cells and inflammation in the brain [80,81], and/or (2) under the presence of hypoperfusion and hypoxia as a result of alcohol-derived brain damage, concentrations of VEGFA might ultimately increase as a compensatory signal in order to form new blood vessels and recruit chemokines to the affected brain area. Here, VEGFA is linked to alcohol abuse.