Given that c-Abl is active in AD, PD, Amyotrophic Lateral Sclerosis (ALS), and Frontotemporal Dementia (FTD) diseases [62,63,64], and that it has also been shown that TFEB overexpression and/or activation is beneficial [22,61,65,66], inhibiting c-Abl in order to increase TFEB in the nucleus could be a therapeutic option for these neurodegenerative and more frequent diseases. Here, ABL1 is linked to amyotrophic lateral sclerosis.