As an example of a comprehensive model of signal transduction, we provide a Wnt network that shows remarkable robustness under a range of phenotypical and pathological conditions. Its simulation allows the clarification of controversially discussed molecular mechanisms of Wnt signalling by predicting wet-lab measurements. A loss of Rac1 (Ras-related C3 botulinum toxin substrate 1) or JNK2 affected the TCF/LEF reporter whereas a loss of JNK1 had only mild effects, likely due to low abundance of JNK1.