It has been reported that approximately 10–15% of tumor cells lengthen telomeres by the alternative lengthening of telomeres (ALT) mechanism, in which TRIM28 protects the telomeric histone methyltransferase SETDB1 from degradation, thereby maintaining the H3K9me3 heterochromatin state of the telomeric DNA, which prevents telomere shortening and reduces telomeric sister chromatid exchange in cells [113]. The gene discussed is TRIM28; the disease is neoplasm.