This may not be surprising, since IKZF1 appears to cooperate with NOTCH1 pathway activation to maintain homoeostasis of monocytic/dendritic progenitors [7] and T-ALL-activating Notch1 mutations in mice frequently coincide with loss-of-function mutations in Ikzf1 [8–11]. The gene discussed is NOTCH1; the disease is acute lymphoblastic leukemia.