The fate of duplicated genes is determined by the interaction of three fundamental forces: mutation, genetic drift and natural selection. The most obvious fate is that one of the duplicates is silenced through deleterious mutations and becomes a pseudogene or disappears from the genome entirely. Some gene pairs are “subfunctionalized” and lose complementary functions, so that both genes are maintained in the genome in order to fulfill the complete function of the ancestral gene. The other fate of duplicated genes is that one copy retains its TWS119 original function while the other becomes “neofunctionalized” acquiring a new adaptive function which is maintained by natural selection. A recent study demonstrated that plant miRNA families are evolving through duplication events similar to those that drive the evolution of protein-coding genes, and that the duplicated copies may acquire divergent expression patterns likely as a result of neo- and subfunctionalization. We speculated that some of the molecular mechanisms might exist in animals as well. Alteration to a duplicated copy of a miRNA gene may impact on its targeting capability, leading to increased or decreased regulatory capacity. Otherwise, one of the miRNA genes might sustain a mutation that changes its targeting capability and drift, while the other would retain its ancestral form and present as conserved animal miRNAs. Under the right circumstances, the mutated duplicate might become favorable selected and eventually fixed in the form of a new miRNA gene. This might be an explanation to that some miRNA family members were lost in one lineage and regained in another lineage. miRNA recognizes its target through the complementarity between seed region and the 39UTR of target gene. Inspection of miRNA families reveals a predominant trend in which duplicated miRNA genes are most similar in their seed regions. However, it should be noted that any change along the length of the mature miRNA is likely to be of some functional impact. That might be an explanation to that most miRNA duplicates only shift their target spectra modestly via changes to the sequence out of the seed region. It is very interesting that miR-33 was previously found in mammals, amphibians, urochordates and several invertebrates, but not in fish. We have discovered two homologs of the human miR-33 in silver carp, their sequences were highly conserved. This is the first report of miR-33 in fish, and we postulate that the spatial and temporal expression of miRNAs may explain the inability of finding miR-33 in other fish studies.