Glycogen synthase kinase 3β (GSK3β) was first identified molecule which acts as a critical mediator of glycogen metabolism and insulin signaling mechanism. The close relation between the dysfunction of GSK3β in diverse diseases affecting public health such as Alzheimer’s disease, inflammation, type II diabetes and cancer, raised the interest on this molecule. GSK3β inhibitors were defined with reducing effects in the pathological symptoms of the mentioned diseases. Epibrassinolide (EBR) as a member of brassinosteroids, a class of plant growth hormones with a similar structure of mammalian steroid hormones, has been shown to induce apoptotic cell death in mammalian cancer cells by our group. In plant, various of GSK3 inhibitors are effective to inhibit GSK3β homologue BIN2. According to the data obtained in our laboratory, EBR treatment caused Ser9 phosphorylation and therefore GSK3β inhibition in epithelial cell lines. We also determined that roscovitine, a cyclin-dependent kinase (CDK) inhibitor exposure to cells was shown to phosphorylate and inhibit GSK3β. Roscovitine acts by competing with ATP for binding at the ATP-binding site of CDK5, therefore it is a drug candidate tested for neurodegenerative disease models. Our research group investigates the molecular mechanism of the potential inhibitor candidates of GSKβ, EBR and/or roscovitine, in Caenorhabditis elegans wild type and mutant models.