Psoriasis and psoriatic arthritis (PsA) are immune-mediated inflammatory diseases with a high burden of disability and increased mortality. The pathogenesis of the disease comprises a dysregulated interaction between stromal and immune cells and a dysfunctional cytokine network supporting chronic inflammation of the skin, entheses and joints. In addition to recent advances in the understanding of TNF blockade, more targets have been discovered delivering insights into the pathogenesis of PsA. This article gives a translational approach by utilizing current clinical development programs providing an insight into the IL-12/IL-23 and the IL-17 axes and also focuses on tissue damage and new small molecules.