Overall, it is thought that normal dermal fibroblasts initially inhibit tumorigenesis via signaling to tumor and immune cells and generating a tumor-limiting ECM, but with intercellular interactions and time, these CAFs become tumor promoting, secrete growth factors, upregulate FAP and NOTCH1, and bind N cadherin (Zhou et al., 2015; LeBleu and Kalluri, 2018). The gene discussed is CDH2; the disease is neoplasm.