In experimental models, LECT2 has been found to impair insulin signaling pathway through phosphorylation of Jun NH2-terminal kinase in C2C12 myocyte [21] and HSP has been shown to contribute to the development of insulin resistance in skeletal muscle via epidermal growth factor receptor/c-Jun N-terminal kinase (EGFR/JNK)-mediated pathway [22]. The gene discussed is LECT2; the disease is Insulin resistance.