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That evening, A. came to the clinic with his parents. Thirteen years old, slim, wearing Chicago Bulls pants and a red wristband with the unmistakable silhouette of Michael Jordan flying towards the rim. He looked shy but alert, not sick at all. His father, 48 years old, sat next to him, just as healthy and calm. Both had been referred to us after a genetic test revealed a truncating mutation in the PKP2 gene, known to be associated with arrhythmogenic right ventricular cardiomyopathy (ARVC).1–3 Two of the father’s cousins had been affected—one had died suddenly, the other had survived a cardiac arrest and now lives with an implantable cardiac defibrillator. When we reviewed their case in our multidisciplinary online team meeting—including sports medicine doctors, heart failure specialists, electrophysiologists—our geneticist, a brilliant colleague and close friend, raised her hands on camera to mime what the ‘asterisk’ meant in the genetic report (‘p.(Gln343*)’): a mutation so severe that hundreds of amino acids were missing from the protein chain. Thus, confirming its pathogenetic potential and its role in one of the leading causes of sudden cardiac death (SCD) in athletes.4–6 However, from the perspective of a clinical cardiologist, all their tests were normal. ECG, echocardiography (including strain analysis, 2D and 3D volumes and function), cardiopulmonary exercise testing (CPET), Holter monitoring, cardiac magnetic resonance (CMR) with and without contrast, serum troponin, NT-proBNP—nothing suggested overt disease. Their hearts were structurally and functionally perfect (figure 1). Importantly, A. and his father were fully asymptomatic and never experienced concerning symptoms like chest pain, dyspnoea and/or dizziness, fainting or syncope. And yet, the discussion inevitably shifted towards risk stratification in genotype-positive and phenotype-negative cases. It is well known that incomplete penetrance does not mean zero penetrance. Specifically, PKP2 gene mutations are among the most studied and described, linked with the possibility to develop the disease.7 8 Exercise, especially high-intensity and competitive activity, has been shown to potentially accelerate the phenotypic expression and adverse outcomes of ARVC in carriers, acting like fuel on a (potential) fire. Following COCIS (Italian consensus) recommendations, and data coming from the literature, we finally agreed to advise against competitive sports participation, even in this entirely phenotype-negative adolescent.