We further investigated the relationship between ERK deactivation and p38 activation under EF-24 treatment and found that EF-24-induced dephosphorylation of ERK and cleavage of caspase-3 and PARP are all significantly reversed by the p38 inhibitor SB203580, suggesting the negative regulation of ERK activity by p38-induced apoptosis of HL-60 AML cells after treatment with a high concentration of EF-24 (2 μM). Here, CASP3 is linked to acute myeloid leukemia.