In summary, the data presented in this article collectively suggest that Col1A2-Cre-(universal)-fibroblasts, through the production of CCN1, are essential for coordinating ECM deposition and neoangiogenesis in the tumor stroma microenvironment and are consistent with the notion that targeting CAFs, and, in particular, matricellular proteins such as CCN1 (20, 86), represents a novel therapeutic target for melanoma. The gene discussed is CCN1; the disease is neoplasm.