Finally, to exclude that the observed signatures were simply tumour signatures and to validate whether Club originated tumours match better with LUAD than AT2 originated ones, we integrated our data with recently published 10× scRNA-seq data of AT2 originating Kras mutant;p53 null tumours55 (Fig. 7d and Supplementary Fig. 7g, h). The gene discussed is KRAS; the disease is neoplasm.