Taken together, our results showed that nearly all CAFs in our breast cancer models originate from tissue-resident mammary fibroblasts and that CD26− NFs are predisposed to become myCAFs, whereas CD26+ NFs are predisposed to become pro-tumorigenic iCAFs, capable of recruiting myeloid cells via CXCL12 secretion and enhancing tumor cell invasion via MMP signaling (Fig. 8H). Here, CXCL12 is linked to neoplasm.