Myeloproliferative Disorders :

They are all associated with the JAK STAT mutation with the exception of CML which is associated with the fusion gene BCR:ABL ( from t(9;22 )-i.e philadelphia chromosome )

CML Tx : imatinib - BCR-ABL Tyrosine kinase inhibitor

TX of the myeloproliferative disorders - Ruxolitinib - Janus kinase inhibitor

I was between these two (cytarabine and imatinib) because I couldn't point out if it was AML or CML. I learned all of the usual clues for each one but I forgot about the fundamental difference of blasts vs mature forms (and that bands are bound to appear in CML too). If they give you a CML in the blast crisis, then look for Auer rods. Anyways, got it wrong and hope that won't happen again.

Now, understanding this I can see how the pharmacology works.

Cytarabine - AML (mostly -blasts and pro-cytes)

Antimetabolite, a purine analog, S-phase specific, inhibit DNA synthesis

Potent enough for the crazy proliferation going on

Imatinib - CML (mostly -cytes and a lot of basophils)

Tyrosine kinase inhibitor of bcr-abl and c-kit tumors

Antimetabolites can also be used, but the best answer is imatinib because it's the most specific for this type of cancer, as it turns off the pro-cancer switch (bcr-abl).