The previously well-established understanding that EGF-stimulated EGFR signaling can induce and/or sustain cellular stemness under both physiological and cancer settings [39, 40], together with aforementioned role of SHCBP1 in EGF-mediated β-catenin activation as evidenced in our current study we were prompted to examine whether SHCBP1 can be involved in regulating the EGF-triggered generation of CSCs in NSCLC. The gene discussed is EGFR; the disease is cancer.