In this study, 2,4-D targeted these kinases with binding energies of −6.5 kcal·mol−1 (for CSNK2A1) and −6.6 kcal·mol−1 (for CSNK2A2), suggesting a potential mechanism for synaptic impairment: Studies utilising a Drosophila model demonstrated that CSNK2A1 regulates DNA damage in both Drosophila and human stem cell-derived neural progenitor cells, identifying potential strategies to ameliorate Alzheimer’s disease (AD)-associated neurodegeneration [34]. This evidence concerns the gene CSNK2A1 and early-onset autosomal dominant Alzheimer disease.