In the case of vitiligo,FOXO3a may interrupt the oxidative pathway by controlling the target gene expression.11 In the case of COPD,FOXO3a may stimulate the expression of Atrogin-1/MAFbx, a biological marker having a pivotal role in the development of COPD.12 On the other hand, the role ofFOXO3a in the case of CGL occurs through establishing the phosphorylation by p210BCR-ABL tyrosine kinase, and may contribute to the proliferation of leukemic progenitors.18,19. This evidence concerns the gene FBXO32 and chronic obstructive pulmonary disease.