  Chronic Myeloid Leukaemia (CML) is a blood-derived proliferative disorder,
which is highly associated to a translocation of chromosomes 9 and 22 or the
creation of Philadelphia chromosome Ph(+) cases, inducing the synthesis of a
chimeric fusion protein, namely BCR-ABL1 (Breakpoint Cluster Region-Abelson 1
chimeric protein), which is known for driving the pathophysiology of the
disease, however variants of CML are also recognized as CML Ph(-), these
nonetheless account for a small percentage of the overall CML patients; posing
thus the question whether BCR-ABL1 fusion protein is required for the whole of
the pathophysiology of CML. Hereof, through a stochastic description, a
discrete time discrete Markov chain depicts the various protein-protein
interactions of BCR-ABL1 to better understand signalling pathways and
time-dependent evolution of these pathways, as well as to provide prospective
therapeutic protein targets to improve both the specificity of the treatment
and the life-expectancy of the patients.
