“…Taken together with various other reports showing that proteasome inhibition reduces platelet aggregation and/or secretion only in presence of low doses of platelet agonists [ 69 , 104 , 108 , 126 , 131 , 149 ], it can be speculated that the proteasome/NF-κB dyad does not regulate platelet activation but rather platelet priming, in which platelets are not fully activated to aggregate (no Ca2+ influx or strong αIIbβ3 activation) but present with activation markers including P-selectin exposure and dynamic cytoskeletal shape changes [ 155 , 156 , 157 ]. Eventually, platelet priming potentiates platelet activation and aggregation when low doses of platelet agonists are secured [ 53 , 133 , 134 , 156 , 158 , 159 ].…”