Heat treatment is capable of inducing HSPA1A expression in several tissues, preventing various obesity-elicited metabolic effects at molecular level, leading to improvement of glucose tolerance, insulin-stimulated glucose transport, and insulin signaling accompanied by the reduction in JNK and IKKβ activities in skeletal muscle [72] and liver [14] of HFD mice, which is almost completely abolished in transgenic HSPA1A+/+ mice [14]. The gene discussed is HSPA1A; the disease is obesity due to melanocortin 4 receptor deficiency.