Together, our GEMM studies support the notion that NPY signaling through NPY1R is required for the metastatic phenotype in KPR172HC cancer cells with no further reduction in metastases to the liver upon whole-body Npy1r knockout compared to the pancreas-specific Npy1r knockout in KPR172HC mice (Fig. 2C compared with Fig. 3C). The gene discussed is NPY1R; the disease is cancer.