A synthetic, cell-permeable, α-helical peptide (SAHM1) has been developed that blocks MAML1 recruitment with high affinity for the interface on the Notch-CSL/RBP-J transactivation complex effectively reducing T-ALL cell line proliferation and Notch-driven progression of leukaemia in a mouse model of T-ALL [307]. This evidence concerns the gene MAML1 and acute lymphoblastic leukemia.