To my knowledge, in lower organisms mechanisms such as MIP (methylation induced post-meiotically) may inhibits repeated sequences by methilation or in other words retroviral or transposable elements jumping. RIP is another mechanism mutating directly the repeated sequences in Neurospora. 

When I carried out genome wide analyses of human cancers such as breast cancer metastases and Glioblastoma (brain tumour), I found many of the CpGs not associated with CpG Island or promoter. They were also associated with gene silencing. Theoretically, they are associated  with silencing retroposons, or other viral derived sequencers in human. But I am not very sure of the methodology to study mechanism of this evolution as I have been more focused on dysregulation/alterations in DNA methylation patterns in tumours either between different subtypes or between normal cells and tumours. 

Dear Vincenzo Rocco and Rajendra Pangeni

Iam sorry to reply too late since I am preparing final exams these days. Thank you for your anwsers! So the methylation of CpG not in CpG island may play an important role in stabilizing human genome right? Many viral derived sequences have the ability to transfer in the genome, and the methylation is one of the method to inhibit this process, protecting the genome (I am not sure whether my understanding is reasonable or not, bu it seems convictive to me).

Later, I also found that the methylation pattern in human genome has been shown associated with aging, thus it is far away from what I proposed before that it is "useless even harmful".

Thank you for your anwsers and time agian!