Although little is known about the role of Bcl-xL in BTZ response in hematologic malignancies, a gradual loss of Bcl-xL, in concert with Noxa upregulation and its increased binding to Bcl-xL, was shown to be necessary for BTZ-induced apoptosis in neuroblastoma cells [43]. The gene discussed is BCL2L1; the disease is hematologic disorder.