Notably, during H1N1 influenza, the levels of vicinal diols, such as 11,12-DiHETrE, 14,15-DiHETrE, 8,9-DiHETrE from AA, and other metabolites produced via the CYP and soluble epoxide hydrolase (sEH) pathways, increase in children with disease progression of H1N1 influenza. The gene discussed is PPIG; the disease is swine influenza.