Since ectopic SET expression antagonised the effects of exogenous PP2A, it is possible that, in CML-BC progenitors, SET-dependent suppression of PP2A activity represents one of the main mechanisms used by BCR/ABL to prevent inactivation of mitogenic and survival signals required for its leukaemogenic activity. The gene discussed is PTPA; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.