In addition, both number and size of tumor formed by transplantation of the spheroids into flanks of the NOD/SCID mice were also increased 10-folds by simultaneous mutations of the two genes.6 The CSC activation by mutant KRas with Apc loss is attributed strongly enhanced activation of β-catenin by its initial activation and its further activation by the stabilized oncogenic KRas by Apc loss followed by activation of the downstream RAF-MEK and ERK cascade (Fig. 5). The gene discussed is KRAS; the disease is neoplasm.