In addition, over-expression of endogenous miR-126 and exogenous miR-126 directly mimic targeting the IRS-1/AKT/ERK or RhoA/ROCK signaling pathways, as well as inhibited CRC cells’ proliferation, migration, and invasion, which resulted in cell cycle arrest, but had no effect on cell apoptosis [93,94]. The gene discussed is AKT1; the disease is colorectal carcinoma.