Consequently, it is possible to hypothesize that chronically elevated blood glucose levels may explain both higher ROCK activation levels and increased plasma angiotensin II levels in treated T2D patients (increased angiotensin levels II are associated with ROCK activation in PMBCs in normotensive rats with genetically induced high ACE levels and angiotensin II and in patients with heart failure) [23, 24]. The gene discussed is ACE; the disease is heart failure.