Moreover, the knowledge that functional inactivation of PP2A tumour suppressor activity occurs in myeloid blast crisis CML through the effect BCR/ABL on SET expression, and that re-establishment of normal PP2A activity antagonises both in vitro and in vivo BCR/ABL leukaemogenesis (see Figure 1), highlights the importance of incorporating PP2A activating drugs (e.g. forskolin) in the current therapeutic protocols for blast crisis and imatinib-resistant (T315I included) CML. The gene discussed is ABL1; the disease is neoplasm.