Focusing first specifically on communication between AF subclusters and their cognate AT2 subclusters (i.e. FMO5+ AT2 with AF-c1/2, CFTR+ AT2 with AF-c3) (Fig. S4A–F) we determined that BMP, EGF, and FGF signaling, known regulators of the AT2 cell lineage, were differentially active between the two niches (Fig. S4C–D). The gene discussed is CFTR; the disease is atrial fibrillation.