We only observed statistically significant increases in glutathione S‐transferase kappa 1 (GSTK1) and glutathione S‐transferase Mu 4 (GSTM4) after 1,25(OH)2D treatment of MG‐63 cells (Fig. 3I), whereby lower levels of GSTK1 have been linked to the elevation of mt ROS underlying hypertrophic cardiomyopathy.(32) Lastly, since the bioinformatics analysis also suggests the downregulation of OXPHOS, we assessed mitochondrial UPR by way of activating transcription factor 5 (ATF5) (Fig. 3J). This evidence concerns the gene CEBPB and hypertrophic cardiomyopathy.