These findings demonstrate indispensable functions for JAK1 signaling in postnatal and adult cardiac maturation and/or function but also suggest JAK1-specific inhibitors, which are widely used in adult patients to treat rheumatoid arthritis and myeloproliferative neoplasms and exhibit a relatively safe cardiac toxicity profile [32–34], could potentially be used to attenuate STAT3-dependent transcription in the stressed heart as a means to antagonize adverse cardiac remodeling. The gene discussed is STAT3; the disease is rheumatoid arthritis.