Apicomplexan parasites such as Plasmodium and Toxoplasma use a unique form of motility to power host cell invasion and egress as well as tissue dissemination. Given that these processes are essential for pararasite pathogenesis understanding how they create force is important. Molecular genetic studies have demonstrated that the ‘glideosome’ is important for parasite motility and consists of a myosin anchored to the parasite periphery by the glideosome associated protein (GAP) complex. The myosin is made up of a unusual ‘type XIV’ myosin, MyoA complexed with two light chains. We are interested in defining how the myosin produces force to drive motility and how the glideosome is linked to the adhesins which bind to the host cell. Here we are using a combination of structural biology, parasite molecular biology and biophysics to understand how force is produced to drive apicomplexan motility.