The improved anticancer effect of HDAC inhibitors enhanced by MEK inhibition can be achieved through diverse mechanisms such as NOXA-mediated Mcl-1 degradation in triple-negative breast cancer [33], c-FLIPL downregulation in B-Raf mutation-positive colon cancer [35], or activation of FOXOs with a subsequent increase in BIM and cell cycle inhibitors in lung cancers harboring a Ras mutation [34]. The gene discussed is BRAF; the disease is triple-negative breast carcinoma.