Some mechanisms have not been previously reported or, if so, have not been emphasized in the SLE literature, including osteoclast differentiation (135), synapse pruning (136, 137), mucin production in goblet and mucous cells (138), leptin signaling pathway (139), gastrin signaling (140), neurotrophin signaling (141, 142), and prolactin receptor signaling (143, 144), which may contribute to the female predominance in lupus. This evidence concerns the gene BDNF and systemic lupus erythematosus.