MCL1 and liver cancer: In view of that (a) a decrease of Mcl-1 is essential for the induction of apoptosis by diverse apoptotic stimuli caused by different types of chemotherapeutic agents; (b) deactivation of ERK may result in Mcl-1 degradation; and (c) the administration of both HDACi and DHA synergistically regulate ERK phosphorylation and Mcl-1 expression, the combination treatment with HDACi and DHA should have a great clinical potential in the improvement of liver cancer treatment.