DNA methylation mostly occurs within the context of CpG dinucleotides and is 
essential for embryonic development and gene repression. It is generally 
accepted that DNA methyltransferases carry out specific and non-overlapping 
functions, Dnmt3a and Dnmt3b being responsible for the establishment of 
methylation around the time of implantation and Dnmt1 ensuring that methylation 
is faithfully copied to daughter cells via what has come to be known as 
"maintenance methylation." This longstanding view has been challenged over the 
years with the observation that Dnmt1 alone is incapable of perfect maintenance 
methylation. A new model is emerging that takes into account a contribution of 
the de novo enzymes Dnmt3a and Dnmt3b in the maintenance of the DNA methylation. 
We recently showed that certain germ line genes are specific targets of Dnmt3b, 
and that Dnmt3b remains bound to their promoter regions in somatic cells via 
interaction with the transcriptional repressor E2F6. It is tempting to consider 
an ongoing role for Dnmt3b in the methylation of germ line genes in somatic 
cells. We propose here observations in support of the hypothesis that the 
maintenance of methylation and subsequent silencing of a handful of germ line 
genes requires Dnmt3b but not Dnmt1. In addition to suggesting a new role for 
Dnmt3b in the protection of somatic cells against the promiscuous expression of 
the germ line program, these observations are of particular interest in the 
field of carcinogenesis, given that the expression of catalytically inactive 
Dnmt3b isoforms and aberrant expression of germ line genes are commonly observed 
in cancer cells.