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Second International ESPT Meeting Lisbon, Portugal, 26–28 September 2013 The second European Society of Pharmacogenomics and Theranostics (ESPT) conference was organized in Lisbon, Portugal, and attracted 250 participants from 37 different countries. The participants could listen to 50 oral presentations, participate in five lunch symposia and were able to view 83 posters and an exhibition. Part 1 of this Conference Scene was presented in the previous issue of Pharmacogenomics. This second part will focus on: clinical implementation of pharmacogenomics tests; transporters and pharmacogenomics; stem cells and other new tools for pharmacogenomics and drug discovery; from system pharmacogenomics to personalized medicine; and, finally, we will discuss the Posters and Awards that were presented at the conference.

After a 1-day advanced course on systems biology, the main themes of this 3-day colloquium were developed: from systems biology to systems medicine with special applications to cancer; pharmacogenomics in drug discovery and clinical application; and epigenomics and genome-wide association studies in cardiovascular diseases. In two roundtable discussions on pharmacogenomics and genome-wide association studies, the progress and the difficulties in the implementation of omics technologies in clinical practice were discussed. Three workshops were also organized on technical tools linked to the meeting themes.

Cardiovascular diseases (CVDs) are a major public health concern ranked by WHO as the number one cause of death globally. Adverse cardiovascular events will largely contribute to the death of almost 23.6 million people a year by 2030 [101]. CVDs are multifactorial pathologies with a significant genetic component. Tremendous breakthroughs in the identification of the genetic variants involved have been made during the last few decades, notably thanks to the technological development of high-throughput genotyping technologies, especially genome-wide association studies (GWAS) [1], as well as the candidategene studies, which have also offered interesting results. However, for most of the variants revealed, the transition from a statistical association to a causal mechanism has proved far from straightforward. Transcriptional analyses meet difficulties in defining the transcripts likely to mediate the associations, thus blocking the translation of genetic discoveries into an improved understanding of disease biology. Moreover, the clinical usefulness of GWAS-identified CVD loci is almost negligible at this stage.