No. Flt3i may be "A" driver mutation, but there are likely many others. NPM1c takes the brakes off of the pTEFb transcription elongation factor which is used my many, many transcription factors. I am reading a paper right now where NPM1c contributes to the upregulation of HOX9a and MEIS1 proteins which by the way are driven by MLL-fusions (another AML lesion). NRAS is liked to the upregulation of mcl-1 (which helps the cell overcome venetoclax).
The bigger point is that those alterations that affect epigenetics combined with NPM1c effect on transcription machinery make the AML cells susceptible to a wide range of drivers.
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