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Leukemic transformation is initiated by specific genomic alterations that impair apoptosis of clonal B\u2010cells.<\/jats:p><jats:p><jats:bold>Diagnosis<\/jats:bold>: The diagnosis is established by blood counts, blood smears, and immunophenotyping of circulating B\u2010lymphocytes, which identify a clonal B\u2010cell population carrying the CD5 antigen as well as B\u2010cell markers.<\/jats:p><jats:p><jats:bold>Prognosis<\/jats:bold>: Two prognostic staging systems exist, the Rai and Binet staging systems, which are established by physical examination and blood counts. Various biological and genetic markers also have prognostic value. Deletions of the short arm of chromosome 17 (<jats:italic>del(17p)<\/jats:italic>) predict resistance to available chemotherapies. Comprehensive prognostic scores are currently being developed.<\/jats:p><jats:p><jats:bold>Therapy<\/jats:bold>: Patients with active or symptomatic disease or with advanced Binet or Rai stages require therapy. For physical fit patients, chemoimmunotherapy with fludarabine, cyclophosphamide, and rituximab remains the current standard therapy. For unfit patients, treatment with an anti\u2010CD20 antibody (obinutuzumab or rituximab or ofatumumab) plus a milder chemotherapy (Chlorambucil) may be applied. At relapse, the initial treatment may be repeated, if the treatment\u2010free interval exceeds two to three years. If the disease relapses earlier, therapy should be changed using alternative agents such as bendamustine (plus rituximab), alemtuzumab, lenalidomide, ofatumumab, ibrutinib, or idelalisib. Patients with a <jats:italic>del(17p)<\/jats:italic> or <jats:italic>TP53<\/jats:italic> mutation can be treated with ibrutinib or a combination of idelalisib and rituximab. An allogeneic SCT may be considered in relapsing patients with <jats:italic>TP53<\/jats:italic> mutations or <jats:italic>del(17p)<\/jats:italic> or patients that are refractory to repeated chemoimmunotherapies.<\/jats:p><jats:p><jats:bold>Future challenges<\/jats:bold>: Several new agents (e.g., ibrutinib, idelalisib, obinutuzumab) hold the potential to improve the outcome of patients with CLL. However, their optimal use (in terms of combination, sequence, and duration) is unknown. Therefore, CLL patients should be treated in clinical trials whenever possible.Am. J. 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