ADAM17 is overexpressed in many human cancers, including lung cancer, whereas genetic or pharmacological ablation of ADAM17 suppressed tumor proliferation and dissemination partly by promoting EGFR ligand release (McGowan et al, 2008; Jiao et al, 2018; Saad et al, 2019a, 2019b; Ni et al, 2020; Schumacher & Rose-John, 2022). Here, EGFR is linked to neoplasm.