Objective: We evaluated the expression of m6A RNA methyltransferases (e.g., METTL3, METTL14, WTAP), demethylases (e.g., FTO and ALKBH5) and reader proteins (YTHDF1-3) in unilateral ureteral obstruction (UUO) model. Furthermore, we incubated human proximal tubular epithelial (HK2) cells under TGFβ treatment as an in vitro model of kidney fibrosis.  Methods: In HK2 cell, m6A RNA methyltransferases (METTL3 and METTL14) and reader protein (YTDHF1) expression increased in dose- and time-dependent manner along with N-cadherin expression by the TGFβ treatment. However, the expression of demethylases (FTO and ALKBH5) was not changed. Also, cellular levels of m6A in both total RNA and mRNA were significantly elevated by the TGFβ treatment. In the UUO model, METTL3 expression and m6A levels in RNAs were significantly increased, but the expression of reader protein and demethylase was not changed. Down-regulation of METTL3 in HK2 cell decreased the expression of TGFβ-induced fibrosis maker such as fibronectin. Methylated RNA immunoprecipitation sequencing (MeRIP-seq) showed several candidate genes which were differentially m6A methylated by TGFβ treatment. In the human CKD tissue, METTL3 elevation, not YTHDF1, was identified compared with healthy control. Results: Alteration of m6A mRNA methylation profile is related to fibrosis in CKD. Modification of m6A mRNA methylation could be a new target for treatment of kidney fibrosis.     Conclusions: Objective: Kidney fibrosis is a final common pathway for chronic kidney disease (CKD). Various intracellular signaling pathways are associated with kidney fibrosis. Recently, N6-methyladenosine (m6A) RNA methylation has been reported to participate in post-transcriptional gene expression regulation. We aimed to investigate the association of m6A RNA methylation and kidney fibrosis. Methods: We evaluated the expression of m6A RNA methyltransferases (e.g., METTL3, METTL14, WTAP), demethylases (e.g., FTO and ALKBH5) and reader proteins (YTHDF1-3) in unilateral ureteral obstruction (UUO) model. Furthermore, we incubated human proximal tubular epithelial (HK2) cells under TGFβ treatment as an in vitro model of kidney fibrosis.  Results: In HK2 cell, m6A RNA methyltransferases (METTL3 and METTL14) and reader protein (YTDHF1) expression increased in dose- and time-dependent manner along with N-cadherin expression by the TGFβ treatment. However, the expression of demethylases (FTO and ALKBH5) was not changed. Also, cellular levels of m6A in both total RNA and mRNA were significantly elevated by the TGFβ treatment. In the UUO model, METTL3 expression and m6A levels in RNAs were significantly increased, but the expression of reader protein and demethylase was not changed. Down-regulation of METTL3 in HK2 cell decreased the expression of TGFβ-induced fibrosis maker such as fibronectin. Methylated RNA immunoprecipitation sequencing (MeRIP-seq) showed several candidate genes which were differentially m6A methylated by TGFβ treatment. In the human CKD tissue, METTL3 elevation, not YTHDF1, was identified compared with healthy control. Conclusions: Alteration of m6A mRNA methylation profile is related to fibrosis in CKD. Modification of m6A mRNA methylation could be a new target for treatment of kidney fibrosis.