Disruption of the circadian rhythms has a profound influence on human health and has been linked to several major diseases, including cancer. It has been demonstrated that the proliferation of tumor cells follows autonomous circadian patterns that are out of phase with nontumor cells. Taniguchi and colleagues have identified that the BMAL1 gene, a major component of the endogenous clock, undergoes promoter CpG island methylation-mediated silencing in hematological malignancies, in which it might prevent the development of the physiological circadian rhythm. These findings suggest a chromatin-based explanation for the lack of rhythmic expression of clock-target genes in tumors, and might be useful for the design of successful chronotherapy strategies. The image shows staining for the BMAL1 protein in unmethylated leukemia cells. For details, see the article by Taniguchi and colleagues on page 8447 of this issue.