Parsing of the relative contribution of BCL-2 and BCL-XL with additional BH3-mimetic drugs ABT199 (BCL-2 specific) and WEHI536 (BCL-XL specific) revealed that together with MCL-1, BCL-XL (rather than BCL-2) is required for tumour cell line monolayer viability and this is not due to compensatory upregulation of BCL-XL in the absence of MCL-1 (Fig. 4A, C). The gene discussed is BCL2L1; the disease is neoplasm.