Gene expression silencing at mRNA level by microRNAs is a well-established form of post-transcriptional regulation.1,2 Such silencing is achieved through microRNA binding to microRNA response elements (MREs) residing mainly in the 3′ untranslated regions of the target mRNA. Over 1000 human microRNAs have been identified,3 and the prevalence of microRNA regulation in a broad range of biological processes and disease often attributes to the fact that a single microRNA can repress hundreds of different mRNAs.4 Interestingly, a single target mRNA often possesses MREs of distinct microRNAs in its 3′ untranslated regions.5 Questions have been raised regarding the need for this redundancy in regulation, and these multiple MREs were once thought to serve as regulatory buffers of different microRNAs. In a recent seminal work, a novel theory, termed the competing endogenous RNA (ceRNA), was proposed to provide a plausible explanation for this interesting phenomenon from a new perspective of gene regulation.6 According to the ceRNA theory, MREs function as letters of this new regulatory system, and ceRNAs, or sets of RNAs including mRNA, pseudogenes, and long noncoding RNAs, can communicate or regulate each other, through competition for common MREs. As such, ceRNA regulatory networks provide a unifying system for regulations among transcriptome-wide RNAs, greatly expanding the functions of RNAs.6 Alteration of this competition between ceRNAs could modify normal state gene expression and in return alter the status of biological pathways to promote an oncogenic program, for example. To that end, a PTEN ceRNA network was uncovered and shown to potentially regulate oncogenesis.6 The fact that this new level of RNA regulations could be prevalent in cells has prompted research to identify ceRNAs of genes related to disease. However, the complexity of ceRNA …