Our investigations revealed that EtOH treatment increased osteoblast necroptosis and decreased osteogenic differentiation and bone formation in vivo; ROS have been considered, at least in part, as a critical driving force for necroptosis; necrostatin-1 and N-acetylcysteine (NAC) ameliorated osteopenia via inhibition of the RIPK1/RIPK3/MLKL signaling pathways. The gene discussed is MLKL; the disease is Osteopenia.