The activity of combining Mtor and histone deacetylase (HDAC) inhibitors, rapamycin and entinostat respectively, chosen to target the mouse tumor susceptibility pathways (p16/Rb and Mtor/PI3K) was found to be synergistic in limiting the growth of a number of B lineage tumor cell lines, including mouse plasma cell tumors, and the human B cell neoplasms, mantle cell lymphoma, and multiple myeloma[20]. Here, CDKN2A is linked to plasma cell myeloma.