In the past decade, our understanding of the pathophysiology of CLL has changed significantly with discoveries such as somatic mutations in the immunoglobulin heavy chain variable region (IGHV) genes, which are associated with a good prognosis [6,7], and lack of IGHV mutations and increased CD38 and ZAP-70 expression, which are associated with poor prognosis. Here, CD38 is linked to B-cell chronic lymphocytic leukemia.