AKT1 and thyroid gland carcinoma: Once CIP treatment indicates that ABI3 is a phosphoprotein (Figure 1B), ABI3 ectopic expression significantly inhibited AKT/GSK3β phosphorylation in thyroid carcinoma cells (Figure 1C and 1D), and phosphorylated form of ABI3 might represent an inactive form of the protein (Figure 3B), we next searched for putative phosphorylation sites using in silico analysis and data available from literature.