However, based on his thrombocytosis and absence of the Ph chromosome at the first diagnosis, we speculate that our patient initially could have harbored CALR mutation, leading to the clinical and histologic manifestations of a Ph− MPN, while the subsequent development of leukocytosis and acquisition of t(9;22)(q34;q11) suggested that CML evolved at a later point in time. This evidence concerns the gene CALR and Increased total leukocyte count.