Gold compounds are a promising class of cytotoxic compounds with significant anticancer potential. Their mode of action is fundamentally different from that of anticancer Pt drugs; however, the mechanistic details are not fully understood and warrant further studies. We have developed a multiomics strategy to reveal the changes induced by a few representative gold drugs in A2780 cancer cells and to decipher their mechanistic implications. This project relies mainly on the combination of proteomics and NMR metabolomics experiments1-3 with additional information arising from metallomics studies and targeted biochemical assays. The combination of the various pieces has provided a fairly complete description of the effects of auranofin (AF) in A2780 cancer cells. The results suggest the occurrence of a "multi-target" mechanism for AF, in which the inhibition of thioredoxin reductase and the induction of oxidative stress represent the main events1. Subsequently, the cellular effects of two cytotoxic gold(I) carbene compounds, i.e. AuNHC and Au(NHC)2, were comparatively analysed in the same cancer cell line, revealing major differences with respect to AF.2 Overall, the applied strategy provides a fairly comprehensive picture of the mode of action of each gold drug tested, highlighting its specificity.