Furthermore, drusen deposits from cases of AMD have been shown to contain amyloid beta40 and some Adam9−/− mice appear to have drusen-like deposits, so it is tempting to consider that loss of ADAM9, a protease with alpha-secretase activity potentially contributing to the nonamyloidogenic pathway of APP processing, could result in an increase in amyloid beta production. The gene discussed is ADAM9; the disease is age-related macular degeneration.