Within, we utilize the mouse prostate cancer cell line Myc-CaP generated from the Hi-Myc murine model of PCa [16], [17] which drives the expression of human c-Myc by the androgen receptor dependent rat probasin promoter to demonstrate that low dose combination of the HDAC inhibitor panobinostat and the mTORC1 inhibitor everolimus in vitro and in vivo result in greater anti-tumor activity than single agent treatment in a murine model of PCa. Here, HDAC9 is linked to prostate cancer.