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'). The gene discussed is PROM1; the disease is Patent ductus arteriosus.