**7. Conclusion**

Despite the achievements of currently used therapy, MM remains difficult to treat. Novel agents such as inhibitors of proteasome or immunomodulatory drugs have prolonged survival of patients with MM and even some patients persist in long term remission. However, there is a little known about mechanisms of myeloma development or the population responsible for the origin and relapse of the disease. Many scientists have tried to explain causes of the relapse but none of their theories have been conclusively confirmed so far. In this review, we explain inconsistencies among particular concepts and the inability to detect cells of origin by the plasticity potential of myeloma PCs. Plasticity of myeloma PCs might be a cause of vast phenotypic heterogeneity of MM and different characteristics of putative myeloma precursors. Under specific signals from aberrant microenvironments, PCs might undergo dedifferentia‐ tion/transdifferentiation changing their phenotype profile, and acquire stem cell-like proper‐ ties to ensure survival. Therefore, an effort to target the specific cell type based only on surface markers is not sufficient. Instead, it is necessary to concentrate on pathologic mechanisms responsible for the transition from non-CSC to CSC like cells. Additional focus on adjacent microenvironments and specific prevention of stem cell-like conversion might increase success of future therapy.
