In line with this hypothesis, Eμ-MYC-driven murine lymphomas are highly responsive to CHK1 inhibitors in transplant models and several human blood cancer cell lines, including Burkitt and Diffuse large B cell lymphomas (DLBCL) respond well to CHK1 inhibition alone or when combined with antimetabolites or ATR inhibitors31–34. The gene discussed is ATR; the disease is lymphoma.