Given that upregulated NF-κB signaling is implicated in the pathogenesis of insulin resistance, avenues to target selectively the IκBβ cascade, leaving the IκBα arm intact, perhaps using a stabilized STX4, could provide a nuanced therapeutic means to limit NF-κB-mediated insulin resistance, muscle degeneration and myofiber death. The gene discussed is INS; the disease is Insulin resistance.