The discovery of the microRNA system has revolutionized our understanding of translational control. Furthermore, growing appreciation of the pivotal role that de novo translation plays in activity-dependent synaptic plasticity has fueled interest among neuroscientists in deciphering how the microRNA system impacts neuronal signaling and the pathophysiology of neuropsychiatric disorders. Although we have a general understanding of how the microRNA system operates, many key questions remain. In particular, the biosynthesis of microRNAs and their role in translational silencing are fairly well understood. However, much less is known about how microRNAs are degraded and silencing is reversed, crucial aspects of microRNA signaling. In contrast to microRNA synthesis which is mediated almost exclusively by a single pathway that culminates in Dicer, recent studies indicate that there are multiple pathways of microRNA degradation that target different subpopulations of microRNAs. While the Lin-28 pathway of microRNA degradation has been investigated extensively, the translin/trax RNase complex has emerged recently as another pathway mediating microRNA degradation. Accordingly, we summarize herein key features of the translin/trax RNase complex as well as important gaps in our understanding of its regulation and function that are the focus of ongoing studies.