Mirodenafil, in an Alzheimer’s disease (AD) model using APP-C105 AD mice, decreased amyloid-beta (Aβ) and tau levels, improved cognitive function, facilitated Aβ clearance through the autophagy-lysosome pathway, enhanced cGMP/PKG/CREB signaling, and supported mitochondrial function [3]. The gene discussed is CREB1; the disease is early-onset autosomal dominant Alzheimer disease.