On the other side, IFN is one of the most potent innate immune responses to prevent viral replication during the early phases of infection [110]. The activation of transcription through JAK/STAT signaling pathway by IFNs leads to the upregulation of several interferon stimulated genes which have the ability to rapidly kill viruses within infected cells [111]. Almost all viruses have developed strategies to combat the effects of type 1 and type 3 IFNs by blocking the IFN signaling pathway [112] and viral encoded factors able to antagonize the JAK/STAT pathway are crucial determinants of virulence [113]. In particular, Influenza A viruses disrupt JAK/STAT signaling by reducing the expression of the IFN receptor and by directly inhibiting IFN signaling [114]. As a consequence, JAK/STAT blockade generated by baricitinib certainly produces an impairment of IFN-mediated anti-viral response, with a potential facilitating effect on the progression of SARS-CoV2 infection at the moment not yet better quantified.