Levesley et al.232have demonstrated that when ABT‐263 (a BCL‐xL inhibitor) is used in combination with MLN8237 (an Aurora kinase inhibitor), it increases the sensitivity of MLN8237 cells, apparently via a BCL‐xL inhibition‐based mechanism. ABT‐263 promotes caspase‐dependent apoptosis and impedes cell division in MLN8237 human glioma and pediatric cell lines.232. The gene discussed is BCL2L1; the disease is central nervous system cancer.