Thus, because of the unique inhibition profile, we hypothesized that TG02 may target both of the pathogenesis aspects of CLL: by blocking Lck and Fyn, TG02 may act as an antagonist to BCR signaling and abrogate the proliferation and surviving signal in the lymphoid tissue microenvironment; by inhibiting CDK9-mediated transcription, TG02 would reduce Mcl-1 and induce apoptosis. This evidence concerns the gene CDK9 and B-cell chronic lymphocytic leukemia.