According to a commentary, this study is essentially another negative trial of a tyrosine kinase inhibitor, joining the long list of targeted therapies that have reported negative outcomes so far in pancreatic cancer. It suggests that although the molecular basis of the mode of action is not completely understood, these trials might have failed because pancreatic cancers display numerous redundant oncogenic signalling pathways, thus identification of additional key signalling hubs driving pancreatic carcinogenesis remains a priority that future strategies should take into consideration. It adds that since pancreatic cancer is a highly heterogeneous disease at the molecular level, identifying subgroups of patients who might benefit from a specific therapy is mandatory. It also notes that post-hoc exploratory analysis of a small cohort suggests a benefit for subgroup of patients who develop a rash, and since EGFR is also expressed in the normal skin, it is not surprising that epidermal side-effects (rash) occur frequently when targeting EGFR. It alludes to many studies that have suggested rash is associated with increased efficacy of anti-EGFR therapy and therefore might be predictive for response, especially in diseases without activating EGFR mutations such as pancreatic cancer. It concludes that although this trial has shown mainly negative results, progress can only be achieved by undertaking well-designed trials that include a comprehensive translational programme aiming to identify predictive biomarkers for molecularly defined subgroups. In addition, future trials testing novel targeted compounds should enroll patients according to predefined and preclinically validated biomarkers.