It has been reported that CTSK is also dramatically and specifically upregulated in patients’ lungs suffered Lymphangioleiomyomatosis (LAM) and LAM‐associated fibroblasts.[54] Considering that the upregulated CTSK could be activated by mTOR signaling while mTOR inhibitor is the only proven treatment for LAM, the upregulated CTSK in LAM could potentially aggravated disease progression. This evidence concerns the gene CTSK and lymphangioleiomyomatosis.