In line with in vivo findings, in both coculture and CM treatment systems, Fgfr4-overexpressing cancer cells strongly induced the expression of CAF markers such as α-SMA and vimentin in NIH/3T3 cells through their secretome, suggesting that the Fgfr4-overexpressing cancer-derived secretome is involved in CAF differentiation (Fig. 2A). The gene discussed is ACTA1; the disease is cancer.