Notably, the marked activation of CYP1A1, CYP1B1, and SLC16A6, coupled with the downregulation of tumour suppressors such as LINC01085 and CBS, underscores the potential of PM2.5 to promote oxidative stress, carcinogenesis, and therapy resistance in a mutation-dependent manner. This evidence concerns the gene CYP1A1 and neoplasm.