It is pathophysiologically straightforward to think that an alteration in the proteins that are part of the desmosome as the desmoplakin complex, due to a variety of stimuli (i.e., parietal stress from exercise, hypertension, toxicity), can trigger the release of pro-inflammatory molecules that initiate and perpetuate an inflammatory response, resulting in myocardial damage. The gene discussed is DSP; the disease is hypertensive disorder.