Enhanced ADAM17 activity mediated by KRAS mutation also facilitates the shedding of S-N (SLC3A2-NRG1) fusion protein NRG1 and the release of soluble NRG1 (sNRG1), which contributes to the increase in ERBB2-ERBB3 heterocomplex receptors and the activation of the downstream PI3K-AKT-mTOR pathway, leading to the growth of lung cancer cells (10). The gene discussed is ADAM17; the disease is lung cancer.