Rossi reported that naive CD4+ T cells activated by ectopic miR-125b exhibited reduced production of IFN-γ and interleukin-13 (IL-13), indicating a reduced effector function of T lymphocytes [29]; this suggested that miR-125b-5p might inhibit the Th1 differentiation of T lymphocytes, and combined with the miR-125b-5p-induced upregulation in M2 macrophages [26], it could partially explain the miR-125b-5p-induced upregulation in ACO as asthma is mainly characterized by the Th2 differentiation pathway. This evidence concerns the gene CD4 and asthma.