ECM is extensively remodeled in tumor progression through 2 main processes: (i) neosynthesis of ECM components (i.e., alternative splicing mechanism of fibronectin to include EDA and EDB domain in malignant tumor fibronectin) and (ii) degradation of ECM by hydrolytic enzymes (e.g., proteases) that are produced, activated or induced by neoplastic cells, therefore become more permissive environment for tumor growth (Kaspar et al., 2006). The gene discussed is FN1; the disease is cancer.