Results: Prominent ETV1 expression was seen in 50 % of GISTs, but no correlation with clinical outcome was found. Correlation of ETV1 expression and KIT mutation was seen in 60 % of cases. MAPKAPK2 overexpression (n =62/ 44.6 %) correlated with pp38 expression (p=0.021) and alterations of chromosome 1 (p=0.024). In one cases with high MAKAPK2 expression, a MAPKAPK2 gene mutation was found. All relapsing GISTs with very low/low risk showed high MAPKAPK2 and KIT expression. MAP-KAPK2 overexpression was an independent prognostic factor for disease free survival (p=0.006). Conclusion: ETV1 is not universally overexpressed in GIST and seems to be induced also by other pathways than KIT-mutation. MAPKAPK2-overexpression is associated with shorter survival in GIST. Patients with low risk GISTs overexpressing MAPKAPK2 might profit from adjuvant tyrosine kinase inhibitor therapy.