In the present invention, inventors have used high throughput sequencing to identify
novel mutations in ABCA1 in CMML patient samples. Further studies in a mouse model of
myelomonocytic leukemia driven by hematopoietic Tet2 deficiency have shown that these
10 somatic mutations abrogate the tumor suppressor function of WT ABCA1, resulting in the
failure to suppress canonical IL3-receptor beta signaling-driven myelopoiesis. The loss of the
myelo-suppressive function of ABCA1 mutants can be overcome by raising HDL levels
through overexpression of the human apolipoprotein A-1 (apoA-1) transgene. Inventors have
also shown that both IL-3Rbeta blocking antibody and cyclodextrin prevented the
15 proliferation of ABCA1 mutant-transduced Tet2 deficient BM cells similar to the effect of
ABCA1-WT overexpression. Accordingly, the invention relates to a method for predicting the
survival time of a subject suffering from CMML comprising the step identifying at least one
ABCA1 and to a method for treating said subject with HDL/ABCA recombinant (ApoA-1);
cylodextrin and/or anti-IL-3Rbeta antibody.