The study revealed that FAP+ CAF exhibited remarkable plasticity, with Detox-iCAF potentially serving as the origin of other subtypes, transitioning into ECM-myCAF and Wound-myCAF via the DPP4 and YAP1/TEAD signaling pathways, respectively, while the TGFβ2/TGFBR2 pathway plays a pivotal role in tumor cell-induced transformation. This evidence concerns the gene YAP1 and neoplasm.