(CCLM) devotes a large section to the cardiac troponins (cTn) and in particular to the impact of the novel high sensitivity (hs) assays on clinical practice. Furthermore, several articles deal with known or novel pitfalls of hs-cTn in clinical diagnostics.While there is no doubt that the hs-cTn assays constitute a significant analytical step forward, they obviously introduced a momentum of uncertainty for many clinicians. Perhaps this is common to all innovations which force people to leave their well known firm ground. In the case of hs-Tn the major changes relate to the rule-in and rule-out criteria of myocardial infarction. Already the first studies have provided robust data that early rule-out can be substantially improved and the ESC has adapted their guidelines accordingly [1][2][3]. However, many clinicians feel that rule-in has become more complicated not to say confusing. Since many of the traditional cTn assays had cut-offs far beyond the 99th percentile due to their relatively high limit of quantitation (LoQ) [4], the positive predictive value of an abnormal test result was high. In fact, it is important to keep in mind that the upper reference limit (URL) of most assays was not the 99th percentile but a significantly higher plasma concentration of cTn [4]. The novel hs-cTn assays provide reliable results between their 99th percentile and the cut-off of their predecessor tests [5]. This opens up a gray zone which was neglected in the past. Interpretation and clinical consequences derived from hs-cTn results in this gray zone are currently debated. For some but not all assays we have thorough data about positive and negative predictive values depending on individual patient characteristics and timing of cTn plasma concentrations [6]. Another issue that is profoundly influenced by the hs-cTn assays is the analysis of changes in cTn plasma concentrations over time and their diagnostic potential [7]. Many traditional cTn assays were not able to provide reliable time courses close to the 99th percentile. Therefore, the use of Δ-cTn generated with these assays was very limited. With the novel hs-cTn assays it is possible to reliably determine Δ-cTn even below the 99th percentile. However, the meaning of such changes is not clear and we will need more data from dedicated studies to interpret them [8][9][10].In order to better appreciate these problems, it is helpful to remember the reasons for the new definition of myocardial infarction introduced in the year 2000 [11]. In the past we tended to differentiate between stable angina, unstable angina, and myocardial infarction. In the 1990s it became clear that patients with unstable angina with elevated cTn concentration had the same risk of adverse outcomes as patients with what was then considered myocardial infarction, while patients without cTn elevations had a much better prognosis [12]. Interestingly, this subgroup of unstable angina patients also benefited from the same interventions as patients with myocardial infarction [13]. This observation finally l...