We focused on a recycling endosome marker protein, insulin-responsive aminopeptidase (IRAP), which has not been reported in platelets. IRAP (Lnpep) gene variants have been reported to be associated with ischemic stroke and septic shock. The regulatory transport of IRAP depends on the cytosolic domain of the enzyme, which has been shown to interact with several proteins involved in vesicle formation or cytoskeleton remodeling; For example, Golgin p115, Vimentin and FHOD1(Formin homologous domain containing protein 1). IRAP has been reported to be involved in mast cell degranulation, dendritic cell phagosomal maturation and TLR9 signaling, and CD3 signaling in T cells.6–9 IRAP enzyme activity is also involved in antigen processing during major histocompatibility complex class I (MHC-I) cross presentation, and its marker endosomes can be degraded by autophagy.