Hypermethylation　of　gene　promoter　has　been　indicated　for　the　contribution　of　gene　silencing,　and　DNA　demethylating　drugs,　such　as　5-aza-2＇-deoxycytidine　(DAC),　has　been　used　clinically　for　cancer　treatment.　However,　the　reason　why　a　proportion　of　genes　with　hypermethylated　promoter　exhibit　high　expression　levels　remains　unclear　and　this　drug　is　not　much　successful　as　expected　in　use.　Furthermore,　CpG　islands　(CGIs)　are　found　to　be　located　in　not　only　promotors,　but　also　in　gene　bodies.　By　RNA-seq　and　reduced　representation　bisulfite　sequencing,　we　found　the　mismatch　between　the　level　of　promoter　methylation　and　gene　expression.　By　chromatin　Immunoprecipitation-quantitative　polymerase　chain　reaction　and　luciferase　reporter　assay,　we　identified　putative　promoters　in　gene　body,　and　proved　the　activities　of　putative　promoters　were　affected　by　the　methylation　level　of　the　CGI　nearby.　DAC　can　reverse　the　DNA　hypermethylation　at　promoter　CGIs　effectively　but　not　the　CGIs　in　gene　body.　We　also　found　that　TET1　could　demethylate　CGIs　both　in　promoter　and　gene　body.　Furthermore,　we　revealed　a　novel　mechanism　that　H3K36me3　could　affect　the　activity　of　putative　promoter,　and　5hmC　recruited　MeCP2　and　CREB1　as　a　coactivator　to　SETD2　promoter,　to　enhance　its　gene　expression　and　result　in　increased　H3K36me3　in　gene　body.　Our　results　concluded　that　putative　promoters　existed　in　the　gene　bodies,　and　TET1　could　influence　the　transcriptional　activity　of　putative　promoters　by　intragenic　demethylation.