Both ectopic expression of miR-548m and knockdown of HDAC6 were able to disrupt the stroma-lymphoma adhesion and consequently induce cell apoptosis, suppress colony formation, sensitize B-lymphoma cells to the cytotoxic drug mitoxantrone, and abolishing the cell adhesion–mediated drug resistance acquisition (CAM-DR) [97]. Here, HDAC6 is linked to lymphoma.