Thus, although it is experimentally feasible to phenotypically alter the ECM and the growth of tumor cells in vivo and in vitro, we now have genotypically complemented a tumor-associated mutation, indicating that replacement of a single gene can restore epithelial differentiation despite multiple genetic abnormalities in a breast cancer cell line and, furthermore, that DEAR1 is a dominant regulator of an important pathway to tumorigenesis in early-onset breast cancer. Here, TRIM62 is linked to neoplasm.