22]. In this study, in vitro treatment of lymphoblastic leukemia cells with Givinostat directly inhibited BCR-ABL signal pathway with significant loss of key phosphoproteins of pBCR-ABL, and pSTAT5 and pCrkL (Figure 1B) in a similar pattern observed in Imatinib-treated CML and K562 [11, 23], but in different mechanisms. Previous studies have shown that the HDAC inhibitor might enhance degradation of BCR-ABL proteins secondary to hyperacetylation of the chaperon protein, HSP90 [24-26]. This evidence concerns the gene HDAC9 and chronic myelogenous leukemia, BCR-ABL1 positive.