Despite the unprecedented clinical success of ibrutinib, resistance mechanisms wherein tumor cells bypass BTK inhibition through acquired BTK mutations (e.g., C481S) and/or activation of alternative survival mechanisms (e.g., PRAS/AKT/mTOR, ERK1/2, NFκB), have rendered ibrutinib ineffective for many patients, imposing the need for novel therapeutics (7). Here, NFKB1 is linked to neoplasm.