Interestingly, upon orthotopic transplantations of mM organoids, En1 depletion resulted in down‐regulation of Vimentin, a mesenchymal marker in the primary tumors and increased CK‐19 positivity in the metastatic PDA cells (Figure S5C, Supporting Information), indicating that EN1 may play a permissive role in the expression of EMT‐related genes in vivo. The gene discussed is VIM; the disease is Patent ductus arteriosus.