Similar to previous studies, we found that PR expressed as a PRU value was an independent predictor of poor prognosis. At ROC analysis, the PRU cutoff value that best discriminated ischemic events tended to be slightly inferior (214 vs. 235 to 240) to previous analyses, but this is consistent with what we previously observed in the 3T/2R (Tailoring Treatment With Tirofiban in Patients Showing Resistance to Aspirin and/or Resistance to Clopidogrel) trial (5- 17), and probably due to a different study population selection. The new important information emerging from the present analysis is the predictive role of PRU assessed at 1 month. By testing on-clopidogrel PR 1 month after index procedure, we significantly improved the ability of PR to discriminate between patients with and without adverse events via a distinct reduction of “false poor responders.” Baseline PRU values are influenced by several confounding factors, particularly acute atherothrombotic events and inflammation. All these factors progressively either reduce their influence or disappear, and then the 1-month evaluation permits us to better discriminate patients with chronic and persistent high on-clopidogrel PR. Moreover, in the early phase, clinical presentation, PCI success, and complications related to procedure or hospitalization might have a stronger impact on short-term outcome than clopidogrel poor response would. Contrarily, in the later phase, all these factors are less important and the “true clopidogrel poor response” emerges as the strongest determinant of poor prognosis. This has relevant clinical implications especially in the context of current ongoing studies trying to identify a “tailored anti-platelet regimen” based on a single baseline PR assessment. Patients labeled as “poor responder” at baseline, who then became full responders after 1 month showed an excellent clinical outcome in our study, which was very close to that of patients who were full responders both at baseline and at 1-month evaluation. Thus, we may speculate that a more aggressive antiplatelet treatment may not be needed and may be even potentially harmful. On the other hand, re-evaluating PRU at 1 month after the index procedure carries several drawbacks, limiting a rapidly tailored approach, avoiding the early treatment of true poor responders, and the prevention of acute and subacute ischemic adverse events. To avoid these limitations, a stratification based on the combination of genotype and phenotype variables may be desirable. In our study population, and similar to previous studies (9), genotype information alone showed lower predictive power as compared with on-clopidogrel PR values, and it was not sufficient to discriminate the majority of patients who would be poor responders at 1 month. On the contrary, by mixing genotype and 2 simple baseline characteristics (on-clopidogrel PR and creatinine clearance), we were able to obtain a new risk score model that was able to predict the majority of poor responders after 1 month and with adverse events. Interestingly, of all clinical parameters, creatinine clearance emerged in our score. Probably, because it includes age, sex, and, in particular, renal function. Impaired renal function is frequent in patients who are elderly and diabetic, which are known factors relating to higher PR. Consistently, recent studies showed lower clopidogrel-induced antiplatelet effects and a greater prevalence of on-clopidogrel high PR in patients with chronic kidney disease (18). The proposed risk score algorithm should be regarded as the first attempt to predict high on-clopidogrel PR at 1 month from baseline variables. Therefore, future larger prospective studies are clearly in demand to evaluate the clinical utility of this or similar risk scores.