In the metaanalysis 41 breast cancer deaths occurred among 85,683 women included in the trials, which translates to 0.96 deaths/10,000 women/year, which is lower than the average number of breast cancer deaths in the general population: 2.26 deaths/10,000 women/year. This demonstrates how selected the participants of the cardiovascular disease prevention trials are in this regard, and the value of population-based studies such as ours. The final proof of statins’ anticancer effects or the lack of such needs to come from clinical trials recruiting specifically cancer patients. The significant mortality decrease in our study was evident already after short-term post-diagnostic statin use. Spontaneous decrease in serum cholesterol has been reported for years before cancer death. Thus lower mortality observed already at the initiation of usage may have been because people dying of breast cancer had less hypercholesterolemia, i.e. indication for statin use. Nevertheless, statins may also have a direct short-term effect on cancer progression as recent clinical trials have demonstrated decreased breast cancer proliferation after just weeks of statin usage. Whatever the reason for the initial mortality benefit between statin users and non-users, the dose-dependent decrease in breast cancer mortality by increasing intensity of usage supports a causal effect. When analyzed separately the risk decrease was not clearly modified by statin potency, as similar risk decrease was observed for high-potent atorvastatin as for other statins. Also hydrophilic pravastatin was associated with a similar decrease as lipophilic statins. This suggests that statins’ anticancer effects in vivo are due to a systemic effect common to all statins, such as cholesterollowering. Our study has several limitations. We could not evaluate whether statins’ effect on mortality was modified by tumor hormone receptor status as this information was unavailable. Neither did we have information on breast cancer screening history, which could have been more common among statin users, possibly causing lead-time bias by earlier breast cancer diagnoses. However, the observed risk decrease even among metastatic cases at diagnosis indicates that lead-time bias may not affect our results to any great Remdesivir degree. Our data lacked information on life-style factors, such as obesity, and usage of medications apart from cholesterol-lowering drugs. It could be assumed that fibrate and resin users are in general similar to statin users regarding these unmeasured factors, yet lower mortality was observed only in statin users. Thus lifestyle factors may not have a great influence on our results.