At the mechanistic level, PAEs such as DEHP, BBP, and DBP specifically activate ERK5 and p38, upregulate AP-1 (c-Fos/c-Jun), enhance expression of proliferation-related genes (Cyclin D1, PCNA), and suppress the cell-cycle inhibitor p21, collectively potentially driving abnormal PCa cell proliferation (Zhu et al., 2018). The gene discussed is JUN; the disease is posterior cortical atrophy.