The human genome contains about 28 million CpG sites, and roughly 60% of the CpG sites are methylated at the 5 position of the cytosine.  During formation of a cancer there is an average reduction of the number of methylated cytosines of about 5% to 20%, or about 840,00 to 3.4 million demethylations of CpG sites.  
DNMT1 methylates CpGs on hemi-methylated DNA during DNA replication. Thus, when a DNA strand has a methylated CpG, and the newly replicated strand during semi-conservative replication lacks a methyl group on the complementary CpG, DNMT1 is normally recruited to the hemimethylated site and adds a methyl group to cytosine in the newly synthesized CpG. However, recruitment of DNMT1 to hemimethylated CpG sites during DNA replication depends on the UHRF1 protein. If UHRF1 does not bind to a hemimethylated CpG site, then DNMT1 is not recruited and cannot methylate the newly synthesized CpG site. The arginine methyltransferase PRMT6 regulates DNA methylation by methylating the arginine at position 2 of histone 3 (H3R2me2a). (See Protein methylation#Arginine.) In the presence of H3R2me2a UHRF1 can not bind to a hemimethylated CpG site, and then DNMT1 is not recruited to the site, and the site remains hemimethylated. Upon further rounds of replication the methylated CpG is passively diluted out. PRMT6 is frequently overexpressed in many types of cancer cells. The overexpression of PRMT6 may be a source of DNA demethylation in cancer.