We have demonstrated that Gs signaling in osterix (Osx)‐expressing osteoprogenitors is required to increase trabecular bone induced by constitutively active PTH1R.(5) Furthermore, mice lacking the α subunit of Gs in osteoprogenitors have severe osteoporosis and do not increase bone mass in response to anabolic (once‐daily) PTH(1‐34).(5, 6) Unexpectedly, osteoblast numbers and bone formation rate increased in response to PTH in male mice,(5) suggesting both Gs‐dependent and ‐independent actions of PTH1R in bone. This evidence concerns the gene PTH and osteoporosis.