However, xenografts derived from VDRKO mammary tumor cells failed to respond to vitamin D analog therapy, indicating that VDR activation is required in the grafted tumor cells for tumor regression (as opposed to host‐derived fibroblasts, adipocytes, endothelial cells, or immune cells that express VDR).(51) In addition, manipulation of either CYP27B1 or CYP24A1 has been shown to alter breast tumor growth in animal models, supporting the idea that cancer cell metabolism of 25D is biologically relevant.(52, 53). The gene discussed is VDR; the disease is breast cancer.