Pancreatic ductal adenocarcinoma (PDAC) still carries a dismal prognosis with overall five-year survival of 8%. Conventional combination chemotherapies are a clear advance in the treatment of PDAC, however subtypes of the disease exist, which exhibit extensive resistance to such therapies. Genomic MYC amplifications represent a distinct subset of PDAC with an aggressive tumor biology. It is clear that hyperactivation of MYC generates dependencies that can be exploited therapeutically. To find MYC-associated dependencies we analyzed human PDAC expression datasets. We observed that MYC is connected to the SUMOylation machinery in PDAC. Components of the SUMO pathway mark a PDAC subtype with worse prognosis and we provide evidence that hyperactivation of MYC is connected to an increased sensitivity to a novel SUMO inhibitor with a potential for further clinical development.