Specificity was assured by several parallel strategies, namely by (i) reducing the concentration of crizotinib to lower doses (≤5 μM) that do not affect ALK-independent lymphomas, (ii) replacing crizotinib by ceritinib, which has a higher potency and specificity for ALK [48], (iii) assuring that genetic inhibition (inducible knockdown) of ALK mirrored the effects of its pharmacological interference, (iv) evaluating crizotinib effects on cells that had become resistant to this inhibitor due to mutation of ALK kinase domain. Here, ALK is linked to lymphoma.