The study [30] investigated the effect of inhaled corticosteroids ciclesonide, cortisone, prednisolone, dexamethasone, and fluticasone on the replication of the MERS-CoV. Among the four compounds, the only ciclesonide was capable of inhibiting viral replication. Also, ciclesonide induced a significant inhibition of viral replication of other human coronaviruses, such as HCoV-229E and SARS-CoV, and another positive-strand RNA virus, rubella virus, while not affect the viral replication of negative-strand RNA viruses, e.g., influenza and respiratory syncytial virus. For the MERS-CoV, a nonstructural protein 15 (NSP15) appeared to act as the target of ciclesonide. An amino acid substitution in the NSP15 conferred resistance of the mutated MERS-CoV to ciclesonide. Mometasone could help deal effectively with the mutated MERS-CoV. For the SARS-CoV2, all three ciclesonide, mometasone, and lopinavir were able to inhibit viral replication to a similar degree. Interestingly, their effect was more noticeable than serine protease inhibitors, e.g., nafamostat and camostat in cells that Vero cells that express TMPRSS2. It indicates the tendency of the SARS-CoV2 to enter the cell through the cathepsin/endosomal pathway rather than through the TMPRSS2/cell surface pathway.