Multiple papers have demonstrated that EGFR is required in pancreatic and lung cancer models driven by oncogenic K-Ras, and that oncogenic Ras activity (GTP-binding) and ERK phosphorylation are substantially reduced by ablation or inhibition of the EGFR, paralleled by reduced tumorigenesis (Ardito et al., 2012; Bardeesy et al., 2005; Dlugosz et al., 1997; Kruspig et al., 2018; Moll et al., 2018; Ponsioen et al., 2021; Sibilia et al., 2000). The gene discussed is KRAS; the disease is lung cancer.