Within the hematopoietic system, for example, KLF4 loss in malignancy leads to accelerated development of NOTCH1-induced T-cell Acute Lymphoblastic Leukemia (T-ALL) by promoting expansion of leukemia-initiating cells and impaired self-renewal and survival of chronic myeloid leukemia (CML) stem/progenitor cells, contributing to impaired maintenance of leukemia in a model of CML-like myeloproliferative neoplasia [131,132,133], and leading to significant reductions in metastasis to the lungs [136]. The gene discussed is KLF4; the disease is leukemia.