Scabies is a skin disease caused by the mite Sarcoptes scabiei, which infects ~100-200 million people worldwide. In the South Pacific and remote Indigenous communities in northern Australia infection rates can be as high as 25-50% of an entire community; children have the highest rates of infection. Although the mite infection itself is rarely lethal, it is highly correlated with secondary bacterial skin infections (S.pyogenes and S.aureus) caused by the severe itching associated with the disease. These secondary infections can directly cause death or result in a range of complications including Glomerulonephritis, Rheumatic Fever and Rheumatic Heart Disease. Current treatments for scabies are broad spectrum anti-parasitics that are mostly topical creams; drug resistance has recently emerged to these compounds. Mass drug administration programs have shown promise, and largely overcome problems of re-infection, however the only current orally available drugs cannot be administered to children. Here we investigate the structure and function of recently discovered Bcl-2-like proteins from the Sarcoptes scabiei genome. We demonstrate that these proteins behave like their human counter parts and may be an attractive target for the development of new treatments that trigger apoptosis to kill mites.