The exact reason for the tumorigenicity by CD138+ cells is unclear, but there are recent reports, by Fuhler et al demonstrating a reduced expression of syndican-1 (CD138) and a change in kinome profile of CD138+ cells, when they interacted with bone marrow stromal cells [33] and by Chaidos et al confirming the existence of an interconvertible tumor propagating population of CD138+ and CD138− cells that are controlled by epigenetic regulators and linked to drug resistance in myeloma patients [34]. Here, SDC1 is linked to neoplasm.