TKIs affect the proto-oncogene c-kit, which affect normal hematopoiesis, resulting in unwanted suppression of progenitor stem cells [8]. With continuation of effective therapy, normal blood count returns as normal hematopoiesis is restored in the marrow and CML clones are reduced [9]. In patients with aplasia biopsy of bone marrow show significant hypocellularity and fatty tissue without evidence of myelofibrosis [10]. Here, KIT is linked to myelofibrosis.