More often studied is the aberrant promoter hypermethylation, which in contrast to hypomethylation, contributes to tumorigenesis by silencing tumor suppressors such as retinoblastoma (RB), cyclin-dependent kinase inhibitor 2A (CDKN2A, also called p16), mutL homolog-1 (MLH1), von-Hippel-Lindau tumor suppressor (VHL), and breast cancer-associated-1 (BRCA1) (Jones and Baylin, 2002, 2007). This evidence concerns the gene VHL and neoplasm.