Approximately 6% of cTnT and 4% of cTnI are present unbound in the cytoplasm of cardiac myofibrils [79] and can be released rapidly into the circulation following ischemia [80] (with or without necrosis) or in response to myofibrillary stretch/strain, which result in an increase in cell membrane permeability [81]. This evidence concerns the gene TNNI3 and ischemia.