Aspirin produces alteration of platelet function characterized by loss of secondary aggregation in response to ADP or epinephrine, and inhibition of aggregation by collagen. In addition, platelet factor 3 release by these reagents is reduced. A similar platelet lesion was produced by an acetylating agent, acetic anhydride, supporting earlier concepts that aspirin activity against platelets may be a consequence of acetylation. An attempt to identify specific acetylation of platelets with acetyl-1-¹⁴C salicylic acid was unsuccessful. Although platelet uptake of the label was demonstrated, metabolic incorporation of acetate could not be excluded.