We propose that the decrease in PBMCs CCR2 and previously reported elevated CCL2 in our ALS patients [12], [13] may indicate an activation of a negative feedback regulation serving to alleviate the inflammation caused by extravasation of activated monocytes/lymphocytes at the site of CNS injury and denervated neuromuscular junction. Here, CCL2 is linked to amyotrophic lateral sclerosis.