Treatment with a chemical activator of Wnt/β-catenin signaling restored BMEC abnormalities in terms of disrupted tight junctions, barrier impedance and permeability, and VCAM-1 expression in ALS patient (TARDBPN345K/+)-derived EECM-BMEC-like cells. This evidence concerns the gene VCAM1 and amyotrophic lateral sclerosis.