Earlier evidence has shown that lack of PPARγ resulted in increased lethality in mice infected with Influenza virus [30], and H3N2 ifluenza virus infection PPARγ was induced via Fatty Acid Binding Protein 5 (FAPB5) to suppress immune responses [31], supporting the crosstalk of PPARγ with viral infection and innate immune responses. The gene discussed is FABP5; the disease is viral infectious disease.