Targeting Bcl11b via inhibitory approaches might be a promising tool for the treatment of rapidly growing list of cancer types expressing BCL11B. Moreover, the identification of HDAC-interacting domain of Bcl11b as a critical mediator of its activity and the finding that BCL11B-mediated apoptosis resistance can be reversed by HDACi may have important implication for therapeutic interventions against BCL11B-positive tumors. Here, HDAC9 is linked to cancer.