Moreover, in case 5, the high CALR mutation level, concurrent with BCR-ABL fusion in almost 100% of the bone marrow cells, could be another strong argument in favor of the same clone that harbors both genetic alterations, which helped to shift the ET morphology to that of CML.[13]. The gene discussed is CALR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.