Conforming with the previous studies (Uccelli et al. 2012; Boido et al. 2014; Ciervo et al. 2017), intrathecal bm-SC transplantations in FUS (1-358) and SOD1 (G93A) mutant ALS-like mice were found to significantly induce disease-modifying effects; they significantly delayed cachexia, weight loss and motor dysfunction, as well as muscle atrophy and the loss of spinal lumbar motor neuron as seen in placebo-treated transgenic mice. Here, SOD1 is linked to amyotrophic lateral sclerosis.