Furthermore, the enhanced miR-338 expression could mimic the inhibitory effect of casticin on cell proliferation and PI3K/Akt pathway activation, whereas miR-338 inhibition mitigated the function of casticin both in vitro and in vivo, suggesting that casticin might suppress AML development and/or progression by increasing the miR-338 expression and targeting RUNX2-PI3K/Akt signaling pathway. The gene discussed is AKT1; the disease is acute myeloid leukemia.