Moreover, genetic deletion of FAP prior to tumor onset in KRasG12D‐driven model of lung adenocarcinoma and in CT26 tumors, as well as pharmacological inhibition of FAP, reduced cancer cell proliferation via activation of ECM/integrin‐mediated signaling.143 FAP also controlled the secretion of ADAMTS8 and MMP1, the cancer‐specific cleavage of collagens and other secreted proteins.142 To determine how CAFs contribute to the proteolysis of the tumor ECM, the CM of patient‐derived gastric CAFs was compared to that of adjacent tissue‐derived fibroblasts. The gene discussed is FAP; the disease is neoplasm.