We previously reported the following: 1) CKD increases the level of circulating C18:0 through a klotho-dependent mechanism; 2) CKD induces levels of aortic transcriptional ER stress effectors such as ATF4 and CHOP; 3) accumulation of C18:0 induces ER stress, resulting in severe medial calcification in vivo; and 4) global and SMC-specific modulations of ATF4 affect medial calcification in CKD (3, 8, –, 11). This evidence concerns the gene DDIT3 and chronic kidney disease.