Combination therapy also resulted in increased vascular patency (Supplemental Figure 6C) without decreasing general fibrosis (as discerned from levels of α-SMA+ CAFs and fibrillar collagen in the PDA stroma; Supplemental Figure 6, D and E), demonstrating that reducing TAMs derived from bone marrow not only renders PDA susceptible to ICB, but can also surmount aspects of the vascular collapse phenotype that play a key role in driving drug-free sanctuaries in PDA (42). Here, ACTA1 is linked to Patent ductus arteriosus.