For example, the influenza virus notably changes cellular miR-106b, miR-124, and miR-1254 expression in favor of influenza replication by regulating human protease genes (such as ADAMTS7, CPE, DPP3, MST1, and PRSS12), which can cause clinical outcomes ranging from mild upper respiratory infections to severe pneumonia[34]; respiratory syncytial virus (RSV) obviously enhances let-7f expression in the host, which likely contributes to delayed viral clearance and inhibits let-7i and miR-30b expression, thus promoting viral replication[35]. The gene discussed is CPE; the disease is susceptibility to pneumonia measurement.