Initially, reduced expression of BTK, CD52 (a CLL disease activity marker), and CD27 (a memory B cell marker) and diminished chromatin accessibility at NF-κB binding sites were observed, followed by a rapid decrease in the activity of B cell lineage-defining transcription factors (EBF1, FOXM1, IRF4, PAX5, and PU.1), loss of CLL cell identity, and acquisition of a quiescent-like gene signature (upregulation of CXCR4, ZFP36L2, and HMGB2) (62). The gene discussed is SPI1; the disease is B-cell chronic lymphocytic leukemia.