The classic Ph-negative myeloproliferative neoplasms (MPN) are a group of clonalhematopoietic disorders caused by a dysregulated JAK/STAT signal transduction because ofacquired somatic mutations of JAK2, CALR or MPL genes. Chronic inflammation maypredispose to MPN development.SARS-CoV-2 infection displays extreme interindividual clinical variability, ranging fromasymptomatic infection to life-threatening coronavirus disease (COVID-19). Age is a majorrisk factor for severe disease. Male sex and medical comorbidities have minor impact. Itwas demonstrated that at least 3.5% of patients with life-threatening COVID-19 havemonogenic inborn errors of TLR3- or TLR7-dependent type I interferons (IFN-I) immunity.It has also been described that at least 15% of patients with life-threatening COVID-19have neutralizing autoantibodies (AAbs) against IFN-I, that precede SARS-CoV-2 infection.As regard MPN, COVID-19 is associated with a mortality as high as 33%. Patients with MFhad the highest mortality (48%), while patients with ET had the greatest risk of venousthromboembolism (16.7%).In this prospective study, we want to search for AAbs against IFN-I in a cohort of MPNpatients to evaluate their prevalence in the MPN population and to look for clinicalcorrelations, including COVID-19 severity.