Results: In this study, neither immunohistochemistry nor FISH results showed a statistically significant difference between the primary tumors and the tumors which metastasized. Statistical analysis of all tumors together (TMA) revealed only one molecular marker (PTEN), which gave results close to statistical significance. Conclusion: This is the first large study of Brazilian patients for PI3K, PTEN AKT expression by Immunohistochemistry and PTEN using FISH. Expression values for molecular markers chosen did not reach statistical significance, although PTEN values were close. Use of FISH to distinguish metastatic from non metastatic cases also came close to statistical significance. These results suggest that the expression of PTEN in uveal melanoma may be a good topic to investigate further. Objective: Chronic antibody-mediated (CAMR) and chronic T-cell-mediated rejection (CTCMR) represent predominant reason for late graft dysfunction. Both categories share similar morphological features. We ask the question whether there are differences between CAMR and CTCMR on the molecular level. Method: Graft biopsies (>3 M) were performed and evaluated according to the Banff classification. Biopsy specimens with CAMR (n=13), CTCMR (n=9) and from protocol biopsies with normal histology (n=10) were stabilized in the RNA-later. Using the Taqman Low Density Array, the intrarenal expressions of 378 genes relating to immune response (B-cell activation, T-cell activation, chemokines, growth factors, immune regulators and apoptosis) were analyzed. Results: Both categories of chronic rejection were associated with up-regulation of many genes in comparison with the control group: chemokines (CCL4, CCL5, CXCL9, CXCL10, CXCL11), growth factor TGFB1, MHC class II (HLA-DMA, HLA-DMB, HLA-DR, UBD), and in T-cell dependent mechanisms (CD3, CD86, LAG3), including cytotoxic T-cell associated transcripts (GBP1, GZMK). In hierarchical clustering, CAMR and CTCMR gene expression profiles were similar. Conclusion: Chronic rejection very probably involves prolonged cooperation of innate immunity and allospecific immune response. Our study showed that CTCMR and CAMR do not differ on the molecular basis.