Thus, the presence or overexpression of LKB1 diminished the responses of breast cancer cells and precancerous mammary epithelial cells to TGF-β, leading to reduced phosphorylation of Smad2/3 and its transcription activity, whereas knockdown of LKB1 and AMPKα1 resulted in opposite changes and disruption of the acinus structure derived from mammary epithelial cells. This evidence concerns the gene STK11 and breast cancer.