These disruptions impair sodium transport in renal tubules, promote endothelial dysfunction, and exacerbate vascular stiffness, worsening hypertension.56 The initial ER–mitochondria contact initiates marking of the fission points upon which the activated DRP1 will localize to initiate fission via mitochondria adaptor proteins, including Mff, Mid49/Mid51, and Fis1.57 Research supports the role of Drp1-mediated mitochondrial fission in cardiovascular diseases. The gene discussed is DNM1L; the disease is endothelial dysfunction.