In our study, we found that LepR dysfunction protected the mice from the CCH-induced histological damages in the white matter, ameliorating the CCH-stimulated expression of proinflammatory cytokines such as TNF-α and IL-1β, and further upregulated the expression of anti-inflammatory cytokines such as IL-4, IL-10, and IL-1Ra. This evidence concerns the gene LEPR and columnar cell hyperplasia of the breast.