This downregulation of both Phospho1 and Smpd3 was independently found in Kusa 4b10 cells and in young rats exposed to PTH and PTH‐related protein 1 (PTHrP).115, 116 The catabolic effects of continuous PTH on the skeleton are well demonstrated in human conditions such as hyperparathyroidism; however, much research has associated this with the upregulation of osteoclastogenesis through the RANKL/OPG axis.117, 118, 119 These data may indicate, however, a simultaneous mechanism effecting inhibition of bone formation as mediated by PHOSPHO1. This evidence concerns the gene PTH and hyperparathyroidism.