Moreover, in vivo FTY720 treatment inhibited the aberrant AKT activation observed in Tregs from untreated RRMS patients compared to healthy individuals (Figure 5B), but no significant changes were observed in FOXO3A phosphorylation in Tregs from FTY720‐treated compared to untreated RRMS patients (Figure 5C), in agreement with the in vitro data (Figure 2). The gene discussed is AKT1; the disease is relapsing-remitting multiple sclerosis.