First, we tested the level of the autophagy marker LC3-II (the lipid-modified form of LC3, which comprises the three family members MAP1LC3A, MAP1LC3B and MAP1LC3C), by following previously published autophagy guidelines (Klionsky et al., 2016), by western blot (WB) analysis as shown in Fig. 4A. A significant increase in the amount of total LC3-II normalized to β-tubulin was found in ALS-hMSCs as compared to in HC-hMSCs at 24 h post NCS treatment, which was blocked by the presence of 3MeA (Fig. 4A,B). This evidence concerns the gene MAP1LC3A and amyotrophic lateral sclerosis.