In 9.6 kB DMP1‐Cre PTH receptor knockout mice, skeletal effects of continuous hyperparathyroidism (decreased cancellous bone mass, decreased cortical thickness, increased osteoid surface, increased osteoclasts) achieved via chronic PTH infusion were blunted/absent.26 In contrast, in 8 kB DMP1‐Cre PTH receptor knockout mice, skeletal effects of secondary hyperparathyroidism elicited by dietary calcium deficiency were completely normal.28 This evidence concerns the gene DMP1 and hyperparathyroidism.