Kruspig et al. demonstrated through experiments that the initiation and progression of KRAS-driven lung tumors require the involvement of ERBB family receptor tyrosine kinases (RTKs), and inhibition of the ERBB network weakens the activation of a series of downstream signaling proteins (such as pERK, STAT3, etc.), while transient pharmacological inhibition of the ERBB network enhances the therapeutic benefits of MEK inhibitors in the autologous tumor environment. The gene discussed is EGFR; the disease is neoplasm.