## 1 Introduction  
Epitranscriptomics [1] generally attracts broad interest. It involves the post-transcriptional editing of RNA. Since this has not been comprehensively investigated, epistranscriptomics is hardly understood, in spite of its ubiquitous nature. A-to-I RNA editing [2] replaces adenosine with inosine, which is usually regarded as guanine. Thus, A-to-I RNA editing can alter the amino acid sequence of a protein translated from A-to-T edited RNA. Similarly, C-to-U [3] editing replaces cytosine with uracil, which also might result in alterations in amino acid sequences. Although the effects of A-to-I and C-to-U are relatively easy to understand, the other effects of epistranscriptomics are not always easy to understand. Such editing is mediated by various components, including Mettls [4] and Mettll14 [5]--used in the most frequently observed form of RNA editing in transcripts that are believed to affect a wide range of biological processes, ranging from development [6] to diseases [7]. It has been reported to be related to Alzheimer's disease [8] and Parkinson's disease [9]. It is also associated with various cancers [10] and plays several roles in immunity [11].  
N6-methyladenosine also has a relationship with epigenetics. Histone H3 trimethylation at lysine 36 guides m6A RNA modification co-transcriptionally [12]. The m6A of chromosome-associated regulatory RNA regulates chromatin state and transcription [13]. m6A modification controls circular RNA immunity [14].  
In spite of these findings, the mechanism by which m6A affects gene expression profiles is unclear. Although there are many studies, most of them remain association studies. For example, [PERSON] et al. found that m6A increases RNAP II pause, in contrast they did not identify a detailed mechanism, and the studies remained simply identifications of links between RNAP II pausing and the m6A RNA modification [15]. [PERSON] et al. found that m6A on chromosome-associated regulatory RNAs can globally tune chromatin state and transcription; nevertheless, this again remained an association study [13]. [PERSON] et al. found that m6A regulates alternative splicing [16]. [PERSON] et al. found that m6A promotes R-loop formation [17]. In spite of only a few examples of studies on the mechanism that m6A regulates transcription, most of them remained as association studies. In this sense, it is important to find some elements that can affect transcription associated with m6A, even if it is a simple association study. [PERSON] et al. [13] recently found that m6A can regulate transcription through histone modification; however, they did not specify the genes whose expressions were potentially affected by m6A. Histone modification is the addition of small molecules, e.g., methylation and acetylation, to histone tails that control chromatin structures. In this study, we applied tensor decomposition (TD)-based unsupervised feature extraction (FE) [18] in order to identify potential target genes whose expression is affected by m6A through histone modifications. As a result, we identified transcription factors that might be recruited by m6A, biological processes that might include genes whose expression is affected by m6A, and diseases caused by gene expression altered by m6A between mice and humans.