I suspect that it had to do with adverse events that appeared during the trial, but I was never a part of the work, and therefore, did not know anything about why they abandoned it. My work on LRP5, Sclerostin and WNT signaling ended when my group published the original G171V mutation in LRP5 as the cause of high bone mass in the family who had the mutation \cite{Little_2002}. Sclerostin is a physiologic inhibitor of LRP5 and WNT signaling in bone, thus a human sclerostin antibody was thought to be a candidate for development of a bone anabolic agent (by inhibiting the inhibitor). Amgen is developing Rosozumab, another antisclerostin antibody. I have not had anything to do with that work, either. I am awaiting the outcome of the Amgen presentation to the FDA. With regard to the story behind our work; how that impactful work came together, and what were the challenges we faced with the research, the publication process and/or funding. Most of the work we did was volunteer work, with no outside funding. The work started in my lab when a local orthopedist referred a patient to my clinic who was 18 years old, and had been under treatment 2 years for back pain due to a soft tissue injury from an auto accident. He reported that her X-rays “looked funny”. Actually, they indicated she had dense bones. Her DXA showed T-scores of +6.0. Her mother accompanied her, and at age 52, she had T-scores of +6.0. A few days later, her father and younger brother were brought to the clinic, and demonstrated T-scores of >+0.5, entirely normal \cite{Johnson_1997}.