In murine model of ALS, in which human superoxide dismutase 1 (SOD1) with the G93A mutation is expressed under control of the cistronic human SOD1 promotor, the lack of expression of CX3CR1 accelerates ALS-like disease progression leading to a rapid and increased neuronal cell death (Boillee et al., 2006; Cardona et al., 2006; Liu et al., 2019). This evidence concerns the gene CX3CR1 and amyotrophic lateral sclerosis.