Under normal conditions, somatic cells have no detectable telomerase activity, but in cancer cells, TERT is reactivated and can contribute to oncogenesis by establishing a feed-forward signalling loop with NF-κB signalling: TERT is transcriptionally upregulated by NF-κB either directly and/or through MYC; in turn, TERT facilitates p65 in its transcriptional program by enhancing p65 nuclear levels, thereby leading to enhanced expression of NF-κB p65 target genes, including MYC, which is a repressor of P21, a pivotal inhibitor of the cell cycle. This evidence concerns the gene CDKN1A and cancer.