Following the contemporary debate surrounding two alternative perspectives on compliance – enforcement and management – this article suggests an analysis through the lens of the rule of law crisis. Specifically, the financial and techno-managerial strategy developed by the EU for the indirect protection of the rule of law relies on mechanisms that combine characteristics from both the enforcement and management approaches. This article will identify these mechanisms, namely the European Semester, the Conditionality regulation, the European Structural Investment Funds and the Recovery and Resilience Facility, in order to determine their nature, features, and tools for ensuring compliance with the rule of law. The hypothesis of this article relies on the idea that the EU’s tools are characterised by a mismatch between the causes of the identified problems and the chosen solutions. Considering that the deployment of the above measures has not re-established compliance, the EU strategy toes between inducing rule conformity on the one hand and deterring rule of law violations on the other. However, it seems that only the former can restore the rule of law, as the latter is considered ill-equipped to reverse or at least halt instances of backsliding. This mismatch explains why the Justice Scoreboard, the Framework, and the Review Cycle with its Annual Report have not made any difference, and more generally, why management strategies are unfit for dealing with deliberate backsliding.1

RF3 was initially characterized as a factor that stimulates translational termination in an in vitro assay. The factor has a GTP binding site and shows sequence similarity to elongation factors EF-Tu and EF-G. Paradoxically, addition of GTP abolishes RF3 stimulation in the classical termination assay, using stop triplets.

We here show GTP hydrolysis, which is only dependent on the simultaneous presence of RF3 and ribosomes. Applying a new termination assay, which uses a minimessenger RNA instead of separate triplets, we show that GTP in the presence of RF3 stimulates termination at rate-limiting concentrations of RF1. We show that RF3 can substitute for EF-G in RRF-dependent ribosome recycling reactions in vitro. This activity is GTP-dependent. In addition, excess RF3 and RRF in the presence of GTP caused release of nonhydrolyzed fmet-tRNA. This supports previous genetic experiments, showing that RF3 might be involved in ribosomal drop off of peptidyl-tRNA. In contrast to GTP involvement of the above reactions, stimulation of termination with RF2 by RF3 was independent of the presence of GTP. This is consistent with previous studies, indicating that RF3 enhances the affinity of RF2 for the termination complex without GTP hydrolysis. Based on our results, we propose a model of how RF3 might function in translational termination and ribosome recycling.