To investigate smooth muscle contractility in asthma, we applied these high-throughput capabilities to study changes in the contractile phenotype of primary human bronchial smooth muscle cells after treatment with TGF-β1,30 IL-13,31 TNFα,32 IL-1β,33 IL-17A,21 and INFγ,34 a panel of six inflammatory cytokines associated with airway inflammation in asthma and linked to airway smooth muscle contractility in previous literature. The gene discussed is TGFB1; the disease is asthma.