A 58-year-old amateur cyclist (MTB), who was considered fit for competitive sports after a specific medical and cardiologic assessment for sports carried out in October 2011 with ECG (Figure 1) consulted a local cardiology clinic in June 2012 because of an oppressive retrosternal thoracic pain felt the day before during his participation in a competitive race. Some days earlier, he had reported a pre-flu symptomatology which had seriously weakened him. After a brief stay in a hospital cardiology department, the athlete was discharged and the diagnosis was "sub-acute inferolateral myocardial infarction in a dyslipidemic patient". Serial electrocardiographs recorded on that occasion (Figure 2) showed a high ST segment with negative T waves in the inferolateral derivations with an enzymatic increase of CPKMB and T troponin. An echocardiographic examination showed regular left ventricular volume and preserved ejection fraction in presence of ipokinesis of inferior-basal and mid- and lateral basal walls. A further coronarography (Figure 3) was basically negative, without significative endoluminal stenosis, myocardial bridge, or congenital anomalies in the context of a coronarography for right-sided heart failure predominance. The athlete was discharged and required a treatment of statins and anti-aggregants (aspirin and clopidogrel) and was advised to rest. After 2 months, a bicycle ergometer stress test was performed in the same cardiology center and the results were negative. No other etiological hypothesis was suggested, nor was any other imaging examination made, therefore the athlete was diagnosed with ischemic heart disease and was considered unfit to perform in competitive sports (prognosis "quoad vitam"). The athlete came back to us for a visit in August 2012; he asked for an accurate diagnosis for what had happened to him, wanted to understand the triggering event of his supposed myocardial infarction, and, above all, to be informed about risks related to physical activity and to his general and sports-related prognoses. A further electrocardiographic and echocardiographic check showed a clear decrease of T wave negativity in inferior leads and its disappearance in precordial antero-lateral leads, and did not find any significant wall motion or segmental kinetic anomalies, even at an infero-lateral wall level. Thus, the athlete underwent cardiac MR examinations, which, although 2 months later, showed the following: "Presence of hyperin-tense signal on T2w-STIR on the inferior medio-apical wall and the lateral-median wall of the left ventricle, mainly on the intramyocardial and epicardial side. A precocious and belated homozonal enhancement (LGR) extended to the adjacent pericardium is associated to this." In conclusion, the MR context gives initial evidence of myocarditis, with traces of activity and outcomes that are still visible (Figure 4).