To further investigate the contribution of CXCR2 activation by endogenous ligands in ALS neuronal depletion, we exposed both WT and mutant hSOD1-G93A NSC-34 cells to increasing concentrations of the two murine functional homologs of CXCL8, i.e., MIP2α (100 pM, 1 nM, 10 nM, 100 nM, 1 μM) and GROα (1 pg/mL, 10 pg/mL, 100 pg/mL, 1 ng/mL, 10 ng/mL, 100 ng/mL), and assessed cellular viability after 24 h. Here, CXCR2 is linked to amyotrophic lateral sclerosis.