For example, one group demonstrated that a mouse model combining three known AMD risk factors—age, high-fat diet and a particular apolipoprotein E genotype—exhibits disease manifestations that resemble those found in AMD patients, including sub-RPE deposits and drusenoid deposits.53 This same group recently reported that a different mouse model combining advanced age, high-fat diet and decreased CFH also exhibits human AMD-like features.54 These findings confirm that the mechanisms underlying AMD pathogenesis are complex and involve both genetic and environmental factors. This evidence concerns the gene APOE and age-related macular degeneration.