Examination of PDA in both cohorts showed regions of well-differentiated, moderately differentiated, poorly differentiated, and necrotic regions; however, KPC-CCR2–/– mice again showed less high-grade tumor as well as significantly less metastatic burden, but no differences in local invasion, α-SMA+ CAF frequency, or fibrillar collagen deposition, when compared with KPC mice (Figure 4C and Supplemental Figure 5, D–G), suggesting that reduced levels of CCL2-recruited TAMs in PDA slow disease progression and reduce metastatic burden, resulting in longer survival of KPC mice. The gene discussed is CCR2; the disease is Patent ductus arteriosus.