A recent high-profile publication by Sherman et al. [17] utilized different mouse models, including the KPC (K-rasLSL.G12D/+; p53R172H/+; Pdx-1-Cre) model, which resembles human pancreatic tumors in terms of responsiveness to gemcitabine, and showed that the VDR activator—calcipotriol—reverses gene signatures associated with the cancer-promoting, activated pancreatic stellate cells, as well as enhances tumor vascularization and gemcitabine intra-tumoral delivery, leading to an overall reduction in tumor volume. The gene discussed is PDX1; the disease is neoplasm.