The significant (65%) decrease in osteoclasts at the tumor-bone interface of ER+ BMETs observed in the 1D11 treatment group in parallel with profound (92%) inhibition of osteolytic lesion progression recapitulates results found in ER- osteolytic BMET preclinical models treated with the same TGFβ-neutralizing antibody used here [30,31,32]; TGFβR kinase inhibitors [30,31,32]; or with tumor-specific inhibition of Smad-mediated TGFβ signaling [22,27,28,57]. The gene discussed is TGFB1; the disease is neoplasm.