To better illuminate the regulatory role of PNP-AMPK axis in influenza-associated inflammation, we further inhibited AMPK phosphorylation by compound C (a well-defined AMPK antagonist) and found that compound C significantly reduced the anti-inflammation response of PNP inhibition, which was evidenced by a much higher level of IL-6 and TNF-α in PNP-knockdown A549 and BEAS-2B cells (Supplementary Figs. 3e, 4b). The gene discussed is IL6; the disease is influenza.