Interestingly, by generating Wnt-independent tumor organoids, which secreted the Wnt antagonist Sfrp1, Mosa et al. found that Sfrp1 or genetic depletion of β-catenin strongly decreased the number of cancer-associated myofibroblasts (myCAFs: α-SMA+/Acta2+).187 Coculture of this tumor organoid with inflammatory CAFs (iCAFs: IL-6+/Tnfa+/IL-1a+) resulted in the upregulation of Vim and Zeb1, while myCAFs reverse this upregulation,187 indicating that the EMT process could be induced by Sfrp1 and that tumor behaviors were differentially regulated via Wnt signaling pathway in specific CAF subtypes. The gene discussed is ACTA1; the disease is cancer.