ERK1/2 are the only known substrates of MEK1/2 [17], and MEK1/2 inhibition by selumetinib reduced ERK1/2 activity to basal levels, confirming that MEK1/2 is a main activator of ERK1/2, and MEK1/2 inhibition is an effective means of blocking MEK1/2-ERK1/2 pathway in AML-stromal cell co-cultures. This evidence concerns the gene MAPK3 and acute myeloid leukemia.