Consistent with the notion that ECM crosslinking, collagen deposition, and enhanced tissue rigidity activate integrin mechanosignaling,[9] EGFR senses these changes in ECM rigidity.[10] Despite intense investigation, a confounding caveat is the lack of knowledge surrounding how EGFR, or its mutants, interact with the corrupt ECM to promote lung cancer. The gene discussed is EGFR; the disease is lung cancer.