The levels of miR‐101‐3p showed an inverse relationship with the expressions of MALAT1 and the inhibited BC cells. In addition, miR‐101‐3p directly targeted the mTOR/PKM2 pathway. Overexpression of MALAT1 led to a significant decrease in gene levels of miR‐101‐3p and an increase in protein expressions of the mTOR/PKM2 pathway. The inhibition of miR‐101‐3p resulted in the blocking of MALAT1. This evidence concerns the gene MALAT1 and breast cancer.