Collectively, these results suggested that AOM-induced somatic mutations that further activate the Wnt/β-catenin pathway (i.e. gain-of-function mutations in ctnnb1; loss-of-function mutations in Apc), rather than mutations in the Ras-Erk signaling cascade, co-operate with ΔN-Bcat to trigger intestinal tumorigenesis. Here, APC is linked to infectious otitis media.