The Th17 pathway has been linked with refractory therapeutic responses to corticosteroids; severe asthmatic patients whose peripheral lymphocytes release more IL-17 exhibit poorer lung function responses to oral corticosteroids [10] and increased pulmonary IL-22 has been reported in steroid refractory asthma [11] and furthermore, serum IL-26 has also been reported to be elevated in uncontrolled asthma patients [12]. This evidence concerns the gene IL22 and asthma.