Overexpression of miR-29a suppressed proliferation of HCC cells by direct targeting secreted multi-functional matricellular glycoprotein and rich in cysteine (SPARC), wherein inhibited SPARC led to the inactivation of its downstream effector AKT and ultimately reduced activity of mammalian target of rapamycin (mTOR) and extracellular signal-regulated kinase (ERK) [55]. The gene discussed is AKT1; the disease is hepatocellular carcinoma.