For example, FOXO1 overexpression in mice has been shown to promote allergic asthma through macrophage polarization, Th9 (T-helper 9 cell) differentiation, and regulation of IRF4 expression, though inhibition of FOXO1 led to attenuation of immune response and asthmatic inflammation through regulation of IRF4 (60, 61). This evidence concerns the gene IRF4 and allergic asthma.