Similar to KRAS wild type colon cancer, in the absence of constitutively active RAS reduction of upstream input to the MAPK and PI3 kinase signal transduction pathways, EGFR inhibition might have merit as a molecular therapy option which might be improved by the use of select downstream mTOR inhibition considering alternative non-erb receptor ligand activation of the PI3K pathway via increased phosphoinositol-mediated signaling, c-Src or protein kinase C signaling via ERK-mediated release of TSC1/2 and mTORC1 inhibition. The gene discussed is TSC1; the disease is colonic neoplasm.