Increased PI3Kα, rather than PI3Kδ expression and activity in primary bronchial epithelial cells isolated from patients with COPD, was found to underpin increased susceptibility to H3N2 and H1N1 influenza viral infection (32); inhibition of PI3K signaling restored protective antiviral responses and suppressed infection in this setting. The gene discussed is PIK3CD; the disease is chronic obstructive pulmonary disease.