However, the study found that concentrations of hs-cTnT remained unchanged after exercise in patients with and without detectable ischemia [26], supporting that factors (e.g., coronary microvascular dysfunction [27], apoptosis [28, 29], or subclinical abnormalities of cardiac structure or function [30] could induce troponin release) in addition to ischemia contribute significantly to the risk associated with cTnT. This evidence concerns the gene TNNT2 and ischemia.