In the early 1980s, it was discovered that a single mutation in the fruit fly genome could specifically activate all copies of a retrovirus-like element called "Gypsy" in the female germline. The site of the mutations that made these Gypsies "dance" was thus called the "flamenco locus". In 2001, Aravin "et al." proposed that double-stranded (ds) RNA-mediated silencing is implicated in the control of retrotransposons in the germline and by 2003 the idea had emerged that vestiges of transposons might produce dsRNAs required for the silencing of "live" transposons. Sequencing of the 200,000-bp flamenco locus was difficult, as it turned out to be packed with transposable element fragments (104 insertions of 42 different transposons, including multiple Gypsies), all facing the same direction. Indeed, piRNAs are all found in clusters throughout animal genomes; these clusters may contain as few as ten or many thousands of piRNAs matching different, phased transposon fragments. This led to the idea in 2007 that in germlines a pool of primary piRNAs is processed from long single-stranded transcripts encoded by piRNA clusters in the opposite orientation of the transposons, so that the piRNAs can anneal to and complement the transposon-encoded transcripts, thereby triggering their degradation. Any transposon landing in the correct orientation in such a cluster will make the individual more or less immune to that transposon, and such an advantageous mutation will spread quickly through the population. The original mutations in the flamenco locus inhibited the transcription of the master transcript, thereby deactivating this defense system.