Due to the fact that the oncogenic tyrosin kinase BCR-ABL (for breakpoint cluster region-Abelson) represses LCNR expression, iron-deprivation via the LCN2-LCNR pathway is inactive in BCR-ABL+ CML (chronic myeloid leukemia) cells, rendering them resistant to apoptosis (178). The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.