The concept that CRY1 binding is enriched for motifs associated with malignant progression was further substantiated through known motif analysis using a broad window around the center of binding (500 bp) (Fig. 2d, Supplementary Fig. 2d–e), wherein expected enrichment of circadian regulated factors (CLOCK, BMAL1, E-Box) was complemented by enrichment of cancer-associated transcription factors of PCa relevance, including several with oncogenic activity (e.g., c-Myc, Max, USF1, SP1, ETS factors, HIF-1α)28–34. The gene discussed is SP1; the disease is posterior cortical atrophy.