Elevated expression of miR-19a in human airway-infiltrating T cells of patients with asthma, and miR-19a promoted TH2 cytokine production in the airways and amplified inflammatory signaling by direct targeting of the inositol phosphatase PTEN, the signaling inhibitor SOCS1 and the deubiquitinase A20 24, while miR-19b-1 reduced airway remodeling, airway inflammation and degree of oxidative stress by inhibiting Stat3 signaling through TSLP downregulation in a mouse asthma model25. This evidence concerns the gene STAT3 and asthma.