In a mouse model of pancreatic adenocarcinoma, a combination of FLT3L, XRT and CD40 agonist was used to skew the DC phenotype away from a Th2 and Th17 response toward a Th1 response.50 In a mouse model of BRAF-mutant melanoma, CD103+ cDC1s were essential for an effective anti-PD-L1 response and could be expanded by FLT3L. The gene discussed is BRAF; the disease is pancreatic adenocarcinoma.