The inhibition of angiogenesis (or “tube formation” in vitro) is apparently only one of the underlying mechanisms here, because the therapeutic effects of APN inhibitors (ubenimex and actinonin) which do not depend on neoangiogenesis have also been described for acute or chronic myeloid leukemia (AML and CML) [19]. The gene discussed is ANPEP; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.