However, recent studies suggest that the pathogenesis for the development of SIADH in SARS-CoV-2 pneumonia can be due to the production of proinflammatory cytokines such as interleukin-6, which doubles the production of ADH via direct stimulation of non-osmotic secretion of ADH, and the activation of hypoxic pulmonary vasoconstriction pathway due to direct insult to the alveolar basement membrane. The gene discussed is AVP; the disease is inappropriate ADH syndrome.