n engl j med 369;2 nejm.org july 11, 2013 187 could undergo further randomization into two groups, one with maintenance treatment and the other without it. Second, the current risk-stratification system for APL (low, medium, and high risk) is based only on white-cell count and platelet count.9 With the discovery of new genetic biomarkers, the few patients with APL who have an inferior prognosis among the clinically apparent low-tointermediate-risk group, such as the two patients in the ATRA–arsenic trioxide group who had a relapse in this study, could eventually be predicted.8 This was the case in a previous report in which one of four patients who had a relapse after ATRA–arsenic trioxide–chemotherapy treatment carried, in addition to PML-RARA, a DNMT3A mutation, which is now considered to be a marker of a poor prognosis.10 Third, for those high-risk patients, new trials of more sophisticated therapy are warranted. Early death before the therapeutic agents take effect, often encountered in this group, should be handled with the use of a multidisciplinary approach. For example, chemotherapy and other agents targeting additional genetic defects in malignant cells should be more appropriately incorporated into an ATRA–arsenic trioxide regimen in order to get closer to our goal of curing all patients with APL. Disclosure forms provided by the authors are available with the full text of this article at NEJM.org. From the State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, and Shanghai Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine — both in Shanghai, China.