These results have subsequently been replicated in an animal model of chronic lung infection with Mycoplasma gallisepticum; overexpression of miR-16-5p was able to stop the inflammatory response, exerting its inhibitory effect directly on PI3K kinase, which is a key component in the NF-κB activation cascade, and therefore, for TNF-α production [37]. The gene discussed is NFKB1; the disease is Recurrent lower respiratory tract infections.