Disruption of the nanoscale organization of CD20 followed by development of PCs could explain the results of a study on immune thrombocytopenia patients after RTX medication, which suggests that B cell depletion generates a milieu that promotes the differentiation and settlement of long-lived PCs in the spleen (37, 38). The gene discussed is MS4A1; the disease is autoimmune thrombocytopenic purpura.