B[c]Ph-N6-dA, which is resistant to NER, is subject to TCR; B[a]P-N6-dA is subject to global NER, with the strong possibility that other repair pathways, including TCR, play a role in its removal. NER repairs B[a]P-N6-dA efficiently, permitting reactivation of gene expression. In the absence of global NER, B[a]P-N6-dA is repaired by other pathways, more than likely including TCR. In contrast, B[c]Ph-N6-dA is a very poor substrate for global NER, with TCR mediating its repair to reactivate gene expression.