In IMR-32 cells, CHL1 over-expression increased levels of the differentiation marker—microtubule associated protein 2 (MAP2), upregulated autophagy, apoptosis, inhibited cell growth, and anchorage-independent colony formation, reduced the activation of RAC and CDC42, decreased the phosphorylation of P38/JNK, AKT, impaired migration and invasion, and reduced orthotopic tumor growth in mice. The gene discussed is AKT1; the disease is neoplasm.