A new approach for disarming Mcl-1 in cancer identified an allosteric mechanism able to disrupt the binding activity of Mcl-1 to BH3 domain of pro-apoptotic proteins: allosteric Mcl-1 inhibitors specifically target Cysteine 286, inducing conformational changes and allosteric inhibition of BH3 domain interaction with Mcl-1 [170], or bind to Lysine 234 allowing specific increase in binding to Mcl-1 over other Bcl-2 family members [171]. The gene discussed is BCL2; the disease is cancer.