KRAS and neoplasm: Taking advantage of cell lineage specific cre lines for the secretory epithelium of the upper airways (CC10-cre, [10]), we recently showed that while activation of β-catenin alone using the Ctnnb1Δ(ex3) mice which will delete important regulatory phosphorylation sites within β-catenin that inhibit its function in Wnt signaling upon cre mediated recombination, has little effect on lung tumor formation, co-activation of both oncogenic K-ras and activated β-catenin leads to far more aggressive tumor formation than when either pathway is activated alone [11].