La Cognata et al. highlighted an upregulation of CXCR2 in both sporadic ALS patients and SOD1G93A mice, showing that treating the mouse models with the CXCR2 allosteric inhibitor Reparixin (Figure 6, panel B), the neuromuscular function of the subjects was improved [44]. Here, CXCR2 is linked to amyotrophic lateral sclerosis.