Because of the WNT signalling-dependent defects observed in 10-week-old Apc2 knockout mice, and the potential role of WNT signalling in driving ovarian tumour development in mice [15, 17, 54, 57, 58], we aged for up to 18 months cohorts of mice in which WNT signalling was activated to different levels using a hypomorphic Apc allele (weak activation of canonical WNT signalling), hypomorphic Apc plus Apc2+/− knockout (moderate activation) or hypomorphic Apc plus Apc2−/− knockout (strong activation). The gene discussed is APC; the disease is ovarian neoplasm.