This should be taken into consideration, because strain differences were recently found to result in altered expression stability of reference genes. Secondly, since all tissue specimens were taken one week postinfarction, it is possible that other optimal reference gene combinations might be more appropriate for other timepoints. We do not exclude the possibility that more optimal reference gene combinations can be found when other stably expressed genes are included in the analysis. However, as evidenced by the low value for the average expression stability value M, our reference gene set outperforms all other reported reference gene sets analyzed so far with the geNorm algorithm in the setting of myocardial infarction. Finally, our findings only apply to the setting of myocardial infarction in mice, and, therefore, do not preclude Gapdh from being an adequate reference gene in other conditions, tissues or species. In conclusion, we identified and validated a stably expressed reference gene set for use in mouse myocardial infarction studies. Optimal reference gene normalization greatly improves statistical significance, power and can dramatically reduce sample size. Our results indicate in particular that Gapdh, which is commonly used for gene expression normalization in myocardial infarction studies, has rather high expression variability in myocardial infarction tissues in mice. We furthermore caution against the use of Gapdh, Polr2a, Actb, B2m and Eef1a1 for gene expression normalization in myocardial infarction studies because of selective up- or downregulation after myocardial infarction. Therefore, inclusion of Gapdh or other suboptimal reference genes will potentially lead to biased gene expression results. Given the risk of inducing reference gene instability when altering experimental conditions, we recommend the validation of a stable set of reference genes as an initial and essential step in all qPCR experiments. Using the SEREX technique we have identified nine antigens that are immunologically recognised by autoantibodies from patients with PTCL, NOS. Four antigens, ODF2, CEP110, RIF1 and RBPJ are also frequently recognised by antibodies in sera taken from healthy control individuals. These represent autoantigens whose immunological recognition is not specifically associated with the presence of lymphoma. Our analysis of the mRNA expression of the remaining five genes, which are preferentially recognised by sera from lymphoma patients, suggests that all are widely expressed in normal tissues. Thus these antigens are unlikely to represent good candidates for lymphoma vaccination, as there may be unwanted side effects on normal somatic tissues. However, this does not exclude the possibility that the five antigens preferentially recognised by sera from patients may have a role in the pathobiology of lymphoma. Two of the antigens were previously uncharacterised, and with the exception of BECN1, none have been previously studied in the ABT-199 context of lymphoma.