Moreover, TDZD-8′s blockade of GSK-3β exerted positive effects in AD and PD by preventing pro-apoptotic signaling cascades associated with neurodegenerative diseases [69], thereby improving motor function [70] and cognitive function [71,72], reversing α-synuclein increase and hyperphosphorylated tau accumulation [73], and disrupting the GSK-3β-regulated Kelch-like ECH-associated protein 1 (Keap1)–nuclear factor erythroid 2-related factor 2 (Nrf2) axis [74]. The gene discussed is KEAP1; the disease is neurodegenerative disease.