When is it warranted to utilize targeted therapies for known mutations (eg. midostaurin or an alternative TKI for FLT3 mutations, ivosidenib for IDH1 mutations, enasidenib for IDH2 mutations, etc)?
Is there benefit in patients without targetable mutations with the use of hypomethylating agents such as azacitidine?
Thank you for your response! In your experience...