The initial lesion for non-hyper mutated/microsatellite stable tumors is adenoma genesis via redundant perturbations in Wnt signaling leading to over expression of β-catenin for which we identified components LRP1B, AC010091.2, CBL, and CBLB. We hypothesize that the guanine nucleotide exchange factors ARHGEF33 and ARHGEF7 may play a similar role to KRAS and NRAS mutations. The gene discussed is KRAS; the disease is adenoma.