Multiple myeloma (MM) reflects the proliferation of terminally differentiated plasma cells with low proliferative capacities, synthesizing monoclonal immunoglobulin (Ig). Tumoral cells are post-germinal centre cells that have been subjected to rearrangement of variable/diversity/joining (VDJ) sequences of Ig heavy chain (IgH) genes, isotype switching and somatic hypermutation. As the result of illegitimate switch recombinations, reciprocal translocations involving the IgH locus located on chromosome 14q32 arise in MM cells with a frequency of 50–70%. Chromosomal translocation results in the cisactivation of candidate oncogenes located on chromosomal partners by enhancer elements within IgH genes. Several recurrent translocations likely relevant to pathogenesis, have been identified: t(11;14)(q13;q32), t(4;14)(p16;q32), t(14;16)(q32;q23), t(6;14)(p25;q32), t(6;14)(p21;q32) targeting cyclin D1/PRAD1/ BCL-1, FGFR3/MMSET, c-Maf, IRF4, cyclin D3, respectively. Analyzing the data of gene expression profiling from 2 different laboratories, Bergsagel and Kuehl reported that MM tumors deregulate at least 1 of the 3 cyclin D genes. They established a classification for subtypes of MM (TC classification, presented in Table I) based both on the presence of a translocation and on the type of expressed cyclin. Indeed, cyclin D1 is present in almost 40% of MM cells lacking the t(11;14), and cyclin D2 exhibited an increased expression in the remaining tumors. This classification could help in predicting prognosis and response to treatments. They proposed that the deregulation of one cyclin D-type renders cells more susceptible to proliferative stimuli and stated that this mechanism is a unifying oncogenic event in MM. All cyclin D-types, acting as sensors of external stimuli, control the G1 and S phases of cell cycle and, in turn, cell proliferation. All cyclin Ds have been recognized as proto-oncogenes, and overexpression of cyclin D1 is commonly observed in human mature B-cell hemopathies. Indeed, in addition to MM, cyclin D1 is overexpressed in more than 90% of mantle cell lymphomas (MCL), all harboring the t(11;14)(q13;q32) activating translocation and in a large subset of hairy cell leukemias (HCL, 50–65%) for which the mechanism of cyclin D1 gene activation is unknown. This review focuses on the role of cyclin D1 in the pathogenesis of MM and underlines some unexpected facts. We present evidence arguing that the presence of cyclin D1 does not give proliferative advantage to tumor cells. As the role of cyclin D1 as a transcriptional regulator is being more documented, we speculate on its involvement in MM pathogenesis.