As the above experiments have demonstrated that S100A9 in neutrophils (a major source) promoted TNFSF13B signals in MM patients, we examined the regulation of TNFSF13B by measuring the surface presence of S100A9 on splenic neutrophils, macrophages, and monocytes after neutrophil depletion in mice (Figures 3A, B). Here, S100A9 is linked to Miyoshi myopathy.