Specifically, treatment with GIST and CAF CM caused resident GFs to adopt a more stellate morphology, and induced the expression of CAF-mediated genes CCL2, RAB3B, and TNC (GSEA; MISHRA_CAF_UP)19, while anti-TGF-β1 blocking antibody treatment inhibited this effect, suggesting that TGF-β1 secreted from tumor cells and CAFs plays an important role for a transition from resident fibroblasts to CAFs. The gene discussed is RAB3B; the disease is neoplasm.