In CRC, augmentation of platelets within a tumor results in activation of c-Jun N-terminal kinases (JNK)/signal transducer and activator of transcription (STAT1) signaling, via binding of p-selectin to p-selectin glycoprotein ligand-1 (PSGL-1) expressed by TAMs; this facilitates activation of the complement component 5a (C5a)/C5a receptor 1 (C5aR1) axis in TAMs and causes their transformation to a tumor phenotype, thereby promoting tumor growth and metastasis. The gene discussed is SELP; the disease is neoplasm.