For example, a mouse model of Sorsby fundus dystrophy, with a Timp3 Ser156Cys knock-in mutation, showed premature age-related changes in Bruch's membrane and RPE, which were evident at 8 months compared with 30 months in wild-type littermates but lacked the most striking features of the human disease, namely massive sub-RPE deposits (resembling those found in L-ORMD), choroidal neovascularization or retinal atrophy [21]. The gene discussed is TIMP3; the disease is Sorsby fundus dystrophy.