Previously, we have reported that the increase of SFAs (16:0 and 18:0) by the reduction of SCD activity in the medial layer of aortas of CKD mice mediates vascular calcification.(15) It has also been reported that 18:1 prevents 16:0-induced atrophy in C2C12 myotubes.(17) In the present study, the increase of SFAs by SCDi in C2C12 myotubes induced muscle atrophy and the excess of ER stress, which were blocked by the co-treatment with 18:1. Here, SCD is linked to chronic kidney disease.