Both can be underlying the efficacy in PTEN deleted tumors.[15] Earlier, the efficacy of SAHA was related to Mcl-1 levels in acute myeloid leukemia.[30] Another study showed that in diffuse large B-cell lymphoma, over-expression of Bcl-2 and Bcl-XL triggered resistance to the HDACi SAHA and Trichostatin A, whereas the Bcl-2 family inhibitor ABT-737 increased sensitivity to SAHA treatment. The gene discussed is BCL2; the disease is diffuse large B-cell lymphoma.