Aengervan et al., for example, reported that individuals with post-exercise cTnI levels above the 99th percentile (>0.040 μg/L) experienced significantly higher rates of a composite endpoint—including all-cause mortality and major adverse CV events ((MACE) encompassing myocardial infarction, stroke, HF, revascularization, or sudden cardiac arrest)—compared to the controls with cTnI levels ≤ 0.040 μg/L (27% vs. 7%, log-rank p < 0.001) [43]. This evidence concerns the gene TNNI3 and Stroke.