Abstract: ?2-Heremans Schmid Glycoprotein (AHSG) inhibits insulin-induced autophosphorylation of the insulin receptor (IR) and IR-tyroskine kinase (TK) activity; genetic ablation of the Ahsg gene enhances insulin signal transduction and increase whole-body insulin sensitivity. Therefor, AHSG and its gene(s) are useful targets for agents that inhibit the development or progression of Type II diabetes or any disease or disorder associated with increased insulin resistance. Provided herein is a method for inhibiting the biological activity of AHSG protein in a cell using compounds that inhibit phosphorylation of AHSG. Also disclosed is a method of augmenting the phosphorylation or IR-TK activity in a liver or muscle cell by providing a compound that lowers the amount of active AHSG or inhibits the biological activity of AHSG. Such effects may be achieved by delivering an antisense nucleic acid construct that hybridizes with AHSG encoding DNA.