In addition, activation of the Kit receptor by SCF leads to the phosphorylation of Akt which is necessary for IL-1-dependent NF-κB transactivation [32], Akt has been postulated to play a role in RA via its ability to regulate NF-κB and also promote resistance to apoptosis through a number of mechanisms [reviewed in [33]]. This evidence concerns the gene KITLG and rheumatoid arthritis.