In summary, our findings suggest that high phosphate reflective of systemic levels encountered in patients with chronic kidney disease induce EndMT in cultured HCAEC through a pathway involving methylation of the RASAL1 CpG island promoter and subsequent transcriptional silencing of the Ras-GTP suppressor RASAL1 and increased intrinsic Ras-GTP activity. This evidence concerns the gene RASAL1 and chronic kidney disease.