On the way to explore the molecular events which dictate the skewing of MΦ function to Th1 bias, we observed enhanced expression and nuclear accumulation of NF-κBp65 and c-jun in ALS treated MΦs whereas NF-κB and AP-1 (a heterodimer of fos and jun or homodimer of jun) activity is hindered in Leishmania infected MΦs29. This evidence concerns the gene NFKB1 and amyotrophic lateral sclerosis.