The possibility to associate a specific cell line to a particular pathology condition would help to better design pharmaceutical studies, in terms of targets such as receptors, channel proteins or enzymes, and biological pathways. It is well-known that under some circumstances expressed genes do not produce the corresponding proteins necessary to exert a specific function. Thus, in continuation with our scientific interests, gene expression related to arachidonic acid (AA) metabolism was looked for in selected HMCLs and the presence of their coding proteins was verified by the western blotting technique. AA metabolism was chosen because, in its very complex network, several eicosanoids, as crucial mediators of several physio-pathological pathways, are produced. Prostaglandin E2 (PGE2), one of the known eicosanoids, is one of the pro-inflammatory and angiogenesis network mediators and supports the growth of several solid tumors [20; 21; 22; 23]. In addition, PGE2 stimulates gene transcription, influences the mitogenesis of normal human bone cells, and promotes tumor metastases formation. Cyclooxygenase (COX) is responsible for PGE2 bio-synthesis from AA, in turn, released from the cell membrane upon mechanical or mitogenstimuli. Both the two known COX isoforms (COX-1 and COX-2) contribute to PGE2 production, even though COX-1 seems to be its major source in normal tissue. COX-1 is also the target of a low dose of acetylsalicylic acid (ASA), the well-known aspirin active principle ingredient that irreversibly inactivates the platelet cyclooxygenase-1 by acetylating its S530, preventing thromboxane formation. In fact, thrombotic complications in patients with newly diagnosed MM treated with lenalidomide, dexamethasone, and thalidomide chemotherapy benefit from aspirin prophylaxis [24; 25; 26]. Tens of millions of worldwide adults take aspirin to reduce their risk of heart attack or stroke. Studies over the last two decades have suggested that regular use of aspirin may have another important benefit: decreasing the risk of developing or dying from some types of cancer [27; 28]. These aspects potentiate the idea that the genes and their encoded proteins involved in the COX-mediated AA cascade would of relevance and noteworthy investigations also in multiple myeloma as in other types of cancer. For this purpose, a microarray data matrix containing the GEP of 40 HMCLs was used. The experiments, here below described, were designed to study a subset of 64 genes that were selected as involved in arachidonic acid metabolism. Particularly, for this purpose, the gene taxonomy proposed by [29] was used, 64 genes were grouped according to their role in arachidonic acid metabolism. Indeed the aim of the analysis was to detect expression patterns possibly connected to different multiple myeloma histotypes, stages, and grades that could emerge from the interaction of the selected genes. The NMF part-based representation was used to reduce the problem dimensionality and to describe the HMCLs as a composition of metagenes (i.e., groups of genes that emerged automatically from data). Finally, the western blotting technique was used to verify if the relationships between genes and HMCLs that have been suggested by NMF were actually coded.