To overcome this replication barrier caused by critical telomere length, cancer cells usually increase the TERT levels and/or TERT activity via (1) TERTp mutations, which increase TERT mRNA levels by creating new ETS binding motifs [15]; (2) amplification of TERT and/or TERC; (3) TERT rearrangement; and/or (4) epigenetic regulation of TERT and its promoter [8]. The gene discussed is TERT; the disease is cancer.