Necrostatin-1-mediated treatment effectively inhibits the RIPK1/RIPK3/MLKL-dependent signaling, and NAC partly prevents the production of ROS and decreases the activation of necroptosis through a positive feedback loop involving RIPK1/RIPK3 and finally ameliorates alcohol-induced osteopenia by reducing osteoblast necroptosis. This evidence concerns the gene MLKL and Osteopenia.