Our results have demonstrated clearly that platelets from the blood of RA patients are dysfunctional and have a reduced ability to respond to the stimulus adequately by promoting α-granule secretion (assessed by P-selectin expression) and exposure of active integrin αIIbβ3 (assessed by the ability to bind fibrinogen) (Table 1 and Figure S1). The gene discussed is SELP; the disease is rheumatoid arthritis.