It is now clear that the chimeric bcr/abl P210bcr/abl fusion protein, which is generated by the reciprocal translocation t(9;22), inhibits apoptosis and increase proliferation. P210bcr/abl plays a central role in the pathophysiology of CML.

• 目前认为CML的主要分子发病基础为:位于9q34的abl基因与位于22q11的bcr基因相互易位形成bcr/abl融合基因,并编码具有很强蛋白酪氨酸激酶活性的P210bcr/abl融合蛋白,该蛋白通过多种信号通路抑制细胞凋亡而导致细胞转化。