Studies have reported that heparin-binding EGF (HB-EGF) can bind to EGFR when mediated by sulfated HSPG, thereby promoting sustained phosphorylation of EGFR on Tyr1068 and Tyr992 residues and activating the downstream AKT and ERK signaling pathways to promote cancer cell proliferation and migration [15]. The gene discussed is AKT1; the disease is cancer.