Conversely, once a combination of environmental stresses acting against a background of genetic susceptibility have resulted in sufficient oxidative stress, CKDN2A is activated, leading to increases in both of its splice products, p16INK4 and p14ARF (Figure 6), the latter of which stabilizes TP53 [65], which not only can induce apoptosis, but is directly associated with age-related cataracts [66]. Here, CDKN2A is linked to Age-related cataract.