SMAD4 and Patent ductus arteriosus: To assess whether overexpression of ERBB2 along with KCST mutations can promote development of clearly invasive PDA from primary human ductal cells, we sorted CD133+ cells from two independent donors (S2 and S3; Supplementary Table 1) and infected with lentiviruses encoding ERBB2 (Fig. 3a) as well as oncogenic KRASG12V and lentiCRISPRs targeting CDKN2A, SMAD4 and TP53 loci (five alterations abbreviated ‘KECST').