For example, 17-AAG, an Hsp90 inhibitor, induced apoptosis and disrupted transcriptional functionality of HIF1α, which is a client protein of Hsp90, and 17-AAG decreased the colony formation ability of mouse lymphoma CSCs and human myeloid leukemia CSCs (Newman et al., 2012). This evidence concerns the gene HIF1A and myeloid leukemia.