How can Chronic myeloid Leukaemic drugs reduce the production of the Philadelphia genotype?
The key is that TKIs, such as Imatinib, are a therapy rather than a cure
Per Wikipedia, Imatinib acts as a competitive inhibitor of the otherwise constitutively-active BCR-ABL fusion protein, rather than the fusion gene.  By binding the kinase domain, BCR-ABL is unable to phosphorylate downstream effectors that result in unchecked proliferation.  As long as a patient continues to take Imatinib, BCR-ABL activity should be blocked.

In the past few years (i.e, long after imatinib's discovery) there has been a lot of research into exactly how hematopoetic stem cells, which reside in the marrow and create leukemic blasts, work. Most HSCs remain in a quiescent state, but it's not particularly well-known how frequently they turn over.  Recent CML studies have shown that after ~5 years, a large portion of CML patients can safely taper the the drug.  Presumably this is related to HSC turnover, but frankly as a leukemia molecular biologist rather than a physician, I'm not the best font of clinical knowledge.