This so-called “BH3-mimetic” drug bound to BCL-2, BCL-XL and BCL-W with low nanomolar affinity and, unlike other putative BCL-2 protein inhibitors described at that time, was able to potently induce mechanism-based (i.e., BAX/BAK-dependent) apoptosis in cell lines, and tumour regression in mouse xenograft models [230,231]. This evidence concerns the gene BCL2L1 and neoplasm.