KRAS and neoplasm: 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.