Based on the properties of the individual components of the nucleolin-β-arr2 chimera and the role of β-arrestin 2 signaling in CML disease progression, we hypothesized that this novel aptamer chimera would selectively inhibit multiple β-arrestin 2-mediated signaling pathways in leukemic cells (Figure 1), thereby blocking their self-renewal capacity. Here, NUCLEOLIN is linked to chronic myelogenous leukemia, BCR-ABL1 positive.