Although it has been demonstrated the existence of active forgetting (AF) mechanisms for several acquired experiences, there is no such evidence of these mechanisms for aversive memories already consolidated. Based on previous work of our group and others we evaluated the participation of different molecular pathways on AF of aversive memories in the ventral tegmental area (VTA) and dorsal hippocampus (HP). We first decided to evaluate if dopamine in the VTA supports AF of aversive memories. However, we found that blocking D1 subtype receptors in the VTA impairs the formation of conditioned place aversion memory and the formation and duration of inhibitory avoidance (IA) memory in a training-dependent manner. Then, we evaluated the role of GABA neurotransmission in the AF of IA memory and found that positive allosteric modulation of GABAA receptors via benzodiazepine systemic administration or infusion in the HP appears not to affect the duration of this memory. Finally, we also recently started to study the role of the GTPase Rac1 in AF of IA memory. Our preliminary results seem to show that the inhibition of this protein in the HP extends the duration of this memory. Until now, we have made an important progress searching for molecular mechanisms that could be mediating AF of consolidated aversive memories. Our results seem to indicate that Rac1 could be mediating this process in the HP and thus open a new range of future studies to advance in the understanding of AF.