TERT and cancer: TERT expression can be reactivated by copy number variants (CNV), TERT or TERTp structural variants, chromosomal rearrangements juxtaposing TERTp to enhancer elements, cellular and viral oncogenes such as Hepatitis B virus (HBV) X protein (HBx) or high-risk Human papillomavirus (HPV)16 and HPV18 E6 oncoprotein, and, last but not least, mutations within TERTp (31% of TERT-expressing cancers) (Figure 1A) [10,30,31,32,33,34,35,36,37,38] (reviewed in [3,4,9,18,19,20,39]).