Transposable elements are genomic parasites that replicate independently from their hosts. They harm their hosts by causing mutations or genomic rearrangements, and most organisms have evolved various mechanisms to suppress their activity. The evolutionary dynamics of transposons in insects, fish, birds and mammals are dramatically different. Mammalian genomes contain few, very abundant but relatively inactive transposon strains, while Drosophila and fish species harbour diverse strains, which typically have low abundance but are much more virulent. We hypothesise that the variation in the diversity and activity of transposable elements between various animal genomes is caused by the differences in the host defence mechanisms against transposon activity. In recent years RNAi, a mechanism capable of gene, virus and transposon silencing has been discovered. We model RNAi as a density dependant mechanism of defence, which can cause competition among transposons depending on its specificity, and test its predictions using the complete Caenorhabditis elegans, Drosophila melanogaster, Fugu rubripes, chicken, mouse, rat and human genome sequences.