In imatinib-sensitive and -resistant (T315I included) BCR/ABL cell lines and in CML-BCCD34+ patient cells, restoration of PP2A phosphates activity, achieved either by using chemical PP2A activators (e.g. forskolin; Feschenko et al, 2002) or by interfering with the SET/PP2A interplay (i.e. PP2Ac overexpression, SET knockdown), promotes BCR/ABL tyrosine dephosphorylation (inactivation) which, in turn, trigger its proteasome-dependent degradation (Neviani et al, 2005). This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.