As miR-155 expression is elevated in neuro-inflammatory pathologies such as MS or ALS [41, 42], our data further suggest that a lack of QKI anti-inflammatory input may result in the deleterious dominance of miR-155 activity, therefore, miR-155-QKI interactions could prove to be significantly important for future therapies aimed at neuro-degenerative pathologies presented with high levels of miR-155. This evidence concerns the gene QKI and amyotrophic lateral sclerosis.