In addition to alterations in claudin and CAM functions, we observed hypermethylation and downregulation of gene products previously hypothesized as suppressors of ovarian tumor progression, including alpha-integrins (possible regulators of cell proliferation and adhesion), carnitine palmitoyltransferase I (CPT1A, a protein believed to play a role in histone deacetylase inhibition), and N-cadherin (CDH2), a member of the cell adhesion proteins often lost during tumor progression [81-84]. The gene discussed is CPT1C; the disease is neoplasm.