Recently, several advances have been made in understanding the pathogenesis of multiple myeloma. Increasing evidence favours a pre-switched, but somatically mutated B-cell as myeloma stem cell to give rise to the malignant clone. Deletions of the p53-gene, partial or total loss of chromosome 13 and rearrangements of band 14q32 and 11q13 are frequently found in multiple myeloma, and were shown to harbour prognostic significance. Presence or absence of distinct chromosomal aberrations may guide selection of treatment strategies in the future. Although melphalan/prednisolone remains the standard of myeloma treatment in elderly patients, significant improvement has been achieved in antimyeloma and in supportive therapy. High dose therapy with autologous stem cell transplantation enhances survival in younger patients and several trials are ongoing to substantiate these results. The effects of interferon maintenance treatment on overall survival is significant in metaanalysis, although the gain achieved is limited. Newer treatment strategies--targeting the molecular level--have just entered clinical trials, and may further improve outcome of myeloma patients.