The observation that inhibition of Chk1 triggers marked ERK1/2 activation, which can be blocked by MEK inhibitors [210] or Ras-targeting agents such as statins [211] or farnesyltransferase inhibitors [212], leading to striking increases in apoptosis and dramatically enhanced lethality, both in vitro and in vivo, along with a requirement for ERK1/2 activation in progression across the G2/M boundary and through mitosis [213], as well as functional roles for MEK/ERK signaling in the DDR [214,215] provide the rationale for combined inhibition of Chk1 and the Ras/Raf/MEK/ERK pathway in AML [90]. This evidence concerns the gene CHEK1 and acute myeloid leukemia.