The results of the phase I study of Navitoclax (ABT-263, disruptor of BCL2–BCL-xL interactions with pro-apoptotic proteins) in patients with relapsed or refractory CLL were more promising, but it caused thrombocytopenia due to BCL-xL inhibition [31, 32]. The gene discussed is BCL2L1; the disease is Thrombocytopenia.