KRAS and neoplasm: These findings suggest that Apc loss-of-function mutations have the capability to initiate polyclonal tumour development through interactions between clonal populations that have sub-optimal activation of pathways associated with oncogenic transformation including that of Kras. To assess whether this capability is dependent on an imbalance in pathway activation between founding cells, the KrasLSL-G12D allele was intercrossed to Villin-creER;Rosafl/Confetti mice and treated with tamoxifen and subsequently ENU.