In addition, this observation well fits with what emerged in the context of other hematological diseases, such as in chronic myeloid leukemia, where the early and rapid reduction of the BCR-ABL1 transcript during treatment with tyrosine kinase inhibitors is associated with a greater probability of obtaining the deep molecular response and prolonged OS [60]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.