As one example among many, colon cancer cells that strongly express EGF/TGF-α (“Epidermal Growth Factor/Transforming Growth Factor-α”) display a resistance to anoikis by at least in part sustaining the activation of Src via autocrine stimulation of EGFR (“EGF Receptor”), therefore allowing Src to maintain functional interactions with Fak and consequently sustaining a Fak/Src-mediated suppression of anoikis [202]. The gene discussed is SRC; the disease is malignant colon neoplasm.