Considering our previous study demonstrated that mTORC1 promotes cathelicidin LL37 production in keratinocytes via a positive feedback loop, which leads to accumulation of LL37 (Deng et al., 2021), we speculate that excess LL37 from keratinocytes induces angiogenesis via activation of mTORC1 signaling in endothelial cells, eventually aggravating the development of rosacea. The gene discussed is CAMP; the disease is rosacea.