IN AML FLT3 IS NOT PREDICTIVE OF RESPONSE TO THERAPY, IT HAS ONLY PROGNOSIS VALUE.

Remember we explained that in good prognosis AML, those that involve Core Binding Factor (CBF), the disruption in this molecule appears to involve disruption of histone deacethylation primarily which an activity of the Beta subunit of the CBF and we showed that the NF-kB was suppressed.  There is an associated  significant depression of cyclins and TNF, TGF which are important for CD135 (FLT 3) receptor entrance into the cell for signal transduction flow to occur. when the FLOW of this pathway is going fine, the receptor decrease at the membrane.  But under lack of TGF, the membrane FLT3 receptor transfer into the cell or its use is decreased causing Mis-location (a well known cellular dysfunction phenomena). Too many FLT-3 lead of course to dimerization and polymerization forming "Tandem" or repeats of FLT-3.
Now FLT3 suppression by growth factor is part of the normal differentiation of cell, or aging of Hematopoietic cells.   Overexpression of the FLT3 as a result confers to the cell dediffentiation and stem cell like characteristics.
The answer of course is now to increase TGF which may not work because Nuclear substrates are already compromised in most cases.  Increase Mesenchymal transformation through MEK is the only option which secondarily will increase VEGF.  Regorafenib provide here the best alternative even though the Sutent have shown activity.  Anti-MEK is the only significant intervention in AML.
Now don't get yourself cocky.  Remember the primary event is Nuclear, so anti-MEK alone cannot solve the issue and could only be for elderly. Give Anti-MEK with the standard Induction regimen and barace yourself for a new panel of side effects.

Another option histone Deacetyl transferase inhibitor and anti-MEK, this may be the chemoth free option!
anti-MEK and Arsenic Trioxide in APL!
Target therapy is here, let's use it!