We then studied the relationship between nilotinib intracellular concentration and its targeting efficiency in primary CML cells (n = 3) by assessing the inhibition of CrkL phosphorylation (pCrkL), as a molecular target of BCR-ABL TK activity, and cell survival after 30 h of incubation with increasing nilotinib concentrations (Fig. 3A,B). The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.