Klotho overexpression in the SOD1G93A mouse model was shown to suppress the production of proinflammatory cytokines, reduce the expression of neuroinflammatory markers, and prevent neuronal loss with a more profound effect in the spinal cord than in the motor cortex, thereby delaying the onset and progression of the disease.58 These results along with the positive effect Klotho has on the promyelinating properties of oligodendrocytes offer compelling evidence in support of developing Klotho-based therapeutic strategies for treating ALS.58 Here, KL is linked to amyotrophic lateral sclerosis.