Accordingly, palmitate-induced insulin resistance in L6 myotubes was found to be dependent on constitutive phosphorylation of STAT 3 and the associated increase in protein expression of SOCS 3 [274], and the ubiquitination and proteosomal degradation of IRS-1 and Akt was demonstrated to contribute to palmitate or NO donor-induced insulin resistance in HepG2 cells and skeletal muscle cells, respectively [245, 275]. The gene discussed is AKT1; the disease is Insulin resistance.