First, we performed histopathologic analysis of individual tumours in animals, where carcinogenesis was induced either by acute CRISPR editing of Apc, causing a truncation at exon 10 (APCex10), or by loss of heterozygosity of Apc in a well-established mouse model of spontaneous intestinal cancer, Apcmin/+ (Fig. 2c–f, Supplementary Fig. S2c–f). The gene discussed is APC; the disease is neoplasm.