Calcipotriol (Cal), a vitamin-D receptor (VDR) ligand, was found to significantly weaken the capacity of CAFs to support tumor growth via transcriptionally deactivating CAFs to a quiescent state with increased lipid droplet storage and decreased expression of fibroblast activation marker α-smooth muscle actin (α-SMA)24,25. The gene discussed is ACTA1; the disease is neoplasm.