In gastric cancer cells, the RANKL/RANK pathway can abrogate cetuximab sensitivity by phosphorylation of EGFR, AKT, and ERK [29], whereas ΔNp63α expression can increase EGFR mRNA, total EGFR protein, and phospho-EGFR (Y1086), thus contributing to tumor cell proliferation [30,31]. The gene discussed is AKT1; the disease is gastric cancer.