Mechanistically, several streams of evidence align with our enrichment signals: experimental systems show that lead activates stress-responsive kinase cascades—including ERK and p38—drives oxidative-inflammatory programs, and induces COX-2 via EGFR-linked and NFAT/NF-κB axes, modules that are canonical oncogenic effectors and overlap with pathways observed in BLCA [49]. Here, MAPK1 is linked to bladder transitional cell carcinoma.