The disclosed data, overall, support the idea that the CRC mouse model APCMin/+ released circulating EV subtypes and other non-vesicular particles with the ability to reprogram and promote pro-tumorigenic activities in human colonic fibroblasts, activating them into a CAF-like state by modulating the classical NF-κB signaling pathway, and then, in turn, these activated CAF derived-secretomes stimulated surrounding normal fibroblasts to acquire a cancer-supportive behavior that might contribute to the initial step for tumor growth development in CRC. The gene discussed is NFKB1; the disease is neoplasm.