The specific altered levels of metals and (metallo-)proteins (i.e., MT1A, S100A6, LF, Fe, Mg and Cu) in the tear film of AMD patients suggest compromised metal homeostasis during the progression of this neurodegenerative disease and may contribute to shedding light into the pathophysiology of macular degeneration. This evidence concerns the gene MT1A and age-related macular degeneration.