Here, we found that the Detox-iCAF cluster can give rise to the activated myCAF state in the presence of cancer cells through two main paths: an indirect transition mediated by the YAP1-signaling pathway passing through the Wound-myCAF cluster and a DPP4-dependent direct transition between Detox-iCAF and ECM-myCAF clusters (see Model, Fig. 8). The gene discussed is DPP4; the disease is cancer.