The high signaling by IL-6 generates high levels of SOCS1 and SOCS3 in tissues sensitive to insulin (Ueki et al., 2004), which impairs the action of this hormone by binding with the IRS-1 and IRS-2, inducing the ubiquitination and degradation of the latter, leading to insulin resistance (Heinrich et al., 2003), a state of hyperglycemia with subsequent compensatory hyperinsulinemia, followed by wasting and claudication and apoptosis of β-pancreatic cells, insulitis, decreased insulin levels, and the generation of DM2. This evidence concerns the gene INS and Hyperinsulinemia.