FLT3 and acute myeloid leukemia: A possible molecular mechanism underlying the accelerated cell growth may be CA4948-induced IRAK1 activation in FLT3 wild-type AML cells, as IRAK4 inhibition can lead to functional compensation of IRAK1 in THP1 cells [31] indicating a requirement for cotargeting IRAK1 and IRAK4 in the treatment of FLT3 wild-type AML.