Ceronie B, et al. - The proposition explored herein was that effective, disease-modifying treatments acted by physical/functional depletion of memory B cells in order to determine if cladribine depleted memory B cells for relapsing multiple sclerosis. Long-term, memory B cell depletion by cladribine was achieved through selective B cell cytotoxicity coupled with slow repopulation kinetics. It was inferred that these possibly served as a new target, with potential biomarker activity, for prospective drug development.