One of the most economically-important fish cultivated in China, the Chinese perch (Siniperca chuatsi), refuses any dead prey fish or artificial diets as they begin to consume the feed. This special food habit markedly increases the production costs and reduces the economic benefits of Chinese perch aquaculture. However, some of these fish can be trained to change their inborn feeding habits to consuming artificial diets after food habit domestication. The roles of phosphoenolpyruvate carboxykinase-1 (pck1) and taste 1 receptor 1 (t1r1) and the possible regulatory mechanism mediated by DNA methylation in food habits transformation were explored. Two groups of mandarin fish were used in the study after domestication: Group W, which consumed live prey fish, and Group C, which consumed artificial diets. The expression levels and DNA methylation status in the upstream region of the transcriptional initiation site of pck1 and t1r1 were detected in the caudal fin, liver, and brain of the fishes from the two groups. The mRNA level of pck1 was significantly higher in the liver than that in the brain and caudal fin (P＜0.05). Methylation of pck1 was generally less frequent in the liver compared with that in the brain and caudal fin; however, the expression levels of pck1 were not necessarily related to the DNA methylation extent in different tissues. For example, compared with caudal fin, the pck1 mRNA levels were relatively higher in the brain; however, some CpG sites were highly methylated. Compared with the caudal fin and liver, a higher expression level of t1r1 was found in the brain (P＜0.05). However, no differences were found in the methylation levels at the CpG sites in these tissues (P＞0.05). Compared with Group W, the expression levels of pck1 were significantly lower in the liver, aligning with a greater extent of methylation at –2169 nt in Group C (P＜0.05). The transcription levels of t1r1 were lower in the brain of Group C (P＜0.05), and the DNA methylation extent did not significantly differ between the two groups at any of the CpG sites in the brain (P＞0.05). Herein, no evidence supported the hypothesis that the DNA methylation status of pck1 and t1r1 in the brain and liver (tissues that can be sampled repeatedly) could be deduced from that in the caudal fin (a tissue that cannot be sampled repeatedly) despite the strong correlations found between the absolute methylation levels in red blood cells (cells that can be sampled repeatedly) and those in the liver, kidney, and brain (tissues that cannot be sampled repeatedly) in previous studies using small songbird. These studies also revealed that the DNA methylation status in the blood cells is a potential biomarker for the DNA methylation status in other tissues. Nonetheless, our results indicate that pck1 and t1r1 might be responsible for the food habit transformation of Chinese perch from consuming live prey fish to artificial diets. Further, the DNA methylation levels in the CpG island of pck1 might be pivotal for fish as their food habits could be successfully transformed into consuming artificial diets via the regulation of pck1 expression. Of note, the DNA methylation of t1r1 may not be the major regulatory factor in food habit transformation. Collectively, our findings enable a better understanding of the role of pck1 and t1r1 in the food habit transformation of Chinese perch and serve as a reference for future research on the genetic regulatory mechanism of food habit transformation in Chinese perch, especially based on DNA methylation.