In pharmaceutical research, scientists have developed various inhibitors and activators to reduce the activities of the Jun NH2-terminal kinase (JNK) and other enzymes that contribute to insulin resistance, such as protein tyrosine phosphatases 1B (PTP1B), fructose-1–6-bisphosphate (FBPase), and glucokinase [192, 193]. This evidence concerns the gene GCK and Insulin resistance.