The letter of Monti et al 1 on covid-19 in patients with chronic arthritis treated with immunosuppressive therapies stimulates some considerations. The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infects cells through the ACE-2 receptor, which is highly expressed in both the lung and the heart. Besides direct tissue injury, SARS-CoV-2 infection can also induce an exaggerated host immune response, frequently inducing a cytokine release syndrome contributing to multiorgan dysfunction. Indeed, high levels of circulating cytokines, particularly interleukin (IL)-6, IL-1β and tumour necrosis factor-alpha (TNFα), are commonly found in patients with covid-19, correlating with mortality (IL-6).2 Current therapeutic strategy involves agents counteracting viral invasion and replication, and inhibitors of cytokine-sustained inflammatory reactions. Indeed, different cytokines involved in the acute inflammatory response are currently targeted by specific medications otherwise employed in the treatment of rheumatic diseases. Agents inhibiting the activity of IL-1β, TNFα, IL-6 and the Janus Kinase 1 and 2 (JAK 1/2)-Signal Transducer and Activator of Transcription (STAT) pathway are currently under consideration in the treatment of covid-19-associated respiratory syndrome.3 We are here providing some arguments to help achieve a more rational therapeutic decision. In any case, as a general consideration, the short-term period of administration of these agents is …