Collectively, our observations that mice deleted for Ccn1 in Col1A2-Cre-(universal) CAFs showed defects in ECM elaboration, angiogenesis, and metastasis, taken in context with our bioinformatic analysis of patient-derived data, implicate an essential pathogenic role for CAF-specific expression of CCN1 in the tumor microenvironment. Here, COL1A2 is linked to neoplasm.