While the functional redundancy among BCL-2, BCL-XL, and Mcl-1 suggests that selective targeting of BCL-2 protein may not lead to extensive cancer cell death, the lack of clinical activity and or excessive toxicity of pan-BCL-2 or dual BCL-2/BCL-XL inhibitors have prompted the development of highly selective inhibitors for individual BCL-2 members. Here, MCL1 is linked to cancer.