In humans, BCR-ABLp185 is associated with a B-ALL phenotype while BCR-ABLp210 is causing CML.[7] However, in mouse models this is very much dependent on the cell type that is used for transduction and transplantation as well as the cytokines included during the in vitro culture.[40] Disease kinetics in both groups was initially very similar, however, the co-expression of SOCS1 and BCR-ABL prolonged disease formation from day 50 onwards. The gene discussed is BCR; the disease is acute lymphoblastic leukemia.