A biofilm is a group of microorganisms sticking to surfaces and secreting extracellular polymeric substances that protect them from outer threats. This allows disease-causing bacteria like the cystic fibrosis pathogens or cells on our teeth, to hide from our immune system until the coast is clear. It also makes these cells up to 1000-fold more resistant to antibiotics. Finding ways to keep microbes from attaching, or to trick them into leaving biofilms, would be highly beneficial for the future of medicine. One trait that inhibits biofilm maturation, but is needed for biofilm dispersal, is their ability to swim. I screened a transposon library of the model archaeon Haloferax volcanii for hypermotility with a new technique, streaking the library down the middle of a low-agar motility plate, allowing me to identify 48 hypermotile mutants by picking mutants that reached the edges of the plates first. Genome analysis reveals that all but one hypermotile mutant contains a tn-insertion or other mutation affecting ,HVO_2248 and/or HVO_1357. While HVO_2248 is a hypothetical protein with no identified conserved domains, HVO_1357 appears to encode the receiver, and its flanking gene HVO_1356, the histidine kinase of a two-component regulatory system. This is exciting because it begins to explain a new archaeal signal transduction pathway that relates to motility. Also, these proteins have the potential to be effective drug targets to prevent biofilm formation or induce the dispersal of cells in an already existing biofilm making them susceptible to antibiotics.