These findings might suggest that PTX3 contributes to AMD development by accelerating RPE cell death, however a non-physiological chemical stimulus (i.e., sodium iodate) was used throughout the study, and the applied experimental setting did not consider the effect of PTX3 on activation of the complement system [a primary pathogenetic mechanism of AMD (Clark and Bishop, 2018)]. This evidence concerns the gene PTX3 and age-related macular degeneration.