By integrating mechanistic data from both experimental and organoid-based studies, it becomes clear that MNPs can disrupt colorectal epithelial integrity, promote oxidative and inflammatory signaling, and interfere with genomic and epigenomic stability—cellular stress responses that plausibly converge on EOCRC-relevant molecular pathways, including TP53 dysfunction, activation of stem-like and proliferative transcriptional programs, and APC-independent WNT signaling, which are central to early tumor initiation. The gene discussed is TP53; the disease is neoplasm.