As expected, higher concentration of imatinib is required in imatinib-resistant CML cells to counteract the constitutive activation of Bcr-Abl in parallel with the hyper-phosphorylation of ERK1/2 and Akt Ser473, while the same concentration is quite ineffective on the phosphorylation extent of rpS6 (Figure 3). This evidence concerns the gene MAPK3 and chronic myelogenous leukemia, BCR-ABL1 positive.