This differential susceptibility suggests that while healthy, polarized cells forming the RPE monolayer in vivo may be resistant to injures leading to an eventual Cer increase, non-polarized, activated RPE cells, frequent in late AMD lesions and in proliferative vitreoretinopathies, might be more susceptible to increased Cer levels resulting from chronic retina injuries (Figure 3). This evidence concerns the gene CBLN1 and proliferative vitreoretinopathy.