miRNA-16 mimic administration can inhibit the expression of the rapamycin-insensitive component of rapamycin targeting protein (Rictor) in human lung fibroblasts, affecting the mammalian target of the rapamycin complex 2 (mTOR C2) signaling pathway, and downregulate the expression of ECM-related proteins, such as secreted protein acidic and rich in cysteine (SPARC), ultimately improving pulmonary fibrosis in vitro and in vivo [28]. Here, SPARC is linked to pulmonary fibrosis.