Genetic modifiers and/or pre-existing mutations in FVB mice may preferentially drive development of claudin-low tumours from Trp53-null luminal cells in our model;alternatively, the FVB background may facilitate acquisition of Yap1 or Met amplification in Trp53-null luminal cells, which cooperates with p53-loss, leading to development of claudin-low mammary tumours. Here, YAP1 is linked to neoplasm.