Conversely, when we performed luciferase assays using a plasmid harbouring the 3’-UTR of FOS and Met mRNAs, in which the binding sites for miR-449a were inactivated by site-directed mutant genesis, the luciferase activity of mutant reporters were unaffected by the simultaneous infection of miR-449a (Fig. 5b). The gene discussed is FOS; the disease is infection.