In addition to mechanisms by which CVD can result in systemic inflammation, there have been multiple mechanisms described by which elevations in IL-6 contribute to MMVD progression, including decreased L-type calcium channel responsiveness, increased oxidative stress, decreased cardiomyocyte energy production and primary pump failure, and ventricular hypertrophy through STAT3 signaling and fibrosis [50]. The gene discussed is STAT3; the disease is cardiac hypertrophy.