In the present work, we found that AKT/mTOR pathway is implicated in AIM2-regulated Gli1 inhibition and EMT progress in CRC cells as evidenced by the fact that AIM2 depletion increased Gli1 protein expression and promoted EMT progress which was reversed by treatment of Ly294002, an indirect inhibitor of AKT. This evidence concerns the gene GLI1 and colorectal carcinoma.