In MNU-induced RP mice [45], TES downregulated the expression levels of Bax and Calpain-2, Conversely, the expression level of Bcl-2 was upregulated after TES treatment, indicating that apoptotic-associated genes were involved in the TES-induced protective effects against MNU toxicity (by qRT-PCR). The gene discussed is BAX; the disease is retinitis pigmentosa 1.