However, recent studies have challenged this paradigm, which instead demonstrated that the activation of ERBB signaling was required for KRASG12D-driven lung tumorigenesis in preclinical mice models and that pan-ERBB inhibition other than EGFR inhibition alone was strikingly effective to inhibit KRAS-mutant tumor growth and progression (61, 62). The gene discussed is EGFR; the disease is neoplasm.