To further support the combined use of Budesonide and Formoterol we show that the two drugs are able to control the cultured Th17 phenotype by reducing the levels of intracellular IL-17A and RORγ(t), and conversely increases the levels of intracellular Foxp3 in T-lymphocytes from children with MA/PR, affecting the subtype CD4+IL-17A+ and CD4+CD25+FoxP3+ T-cells. The gene discussed is FOXP3; the disease is microtia.