Cellular fibronectin that undergoes alternative splicing to include EDA is synthesized by fibroblasts, endothelial cells, myoblasts [15], and osteoblasts [16]; yet EDA-FN splice variant only appears to be expressed with implications in wound repair [17,18], pathological fibrosis [19], and tumor development [20,21,22]. The gene discussed is FN1; the disease is neoplasm.