Consistent with these previous studies, we demonstrated that ectopic overexpression of SPRED1 lead to a decrease of pERK, induction of apoptosis and reduction of proliferation of THP-1 cells; in sharp contrast, silencing of SPRED1 activated ERK signaling, enhanced the proliferation and reduced the apoptosis of OCI-AML3 cells, which highly express SPRED1. Therefore, one of the mechanisms by which SPRED1 functions as a tumor suppressor in AML is to antagonizing Ras-MAPK signaling. Here, RUNX2 is linked to neoplasm.