Other studies revealed common signalling pathways between ALS and cancer, such as Scr/c–abl, which was found to be overactivated during both cancer and ALS progression [20], and the P38 mitogen-activated protein kinase (p38MAPK) pathway [21], whose inhibition rescued the axonal transport defects in ALS mice [22]. The gene discussed is ABL1; the disease is amyotrophic lateral sclerosis.