The inhibitor-induced a reduction of p-IGF-1R and degradation of the IR substrates 1 and 2 (IRS1/2) leading to the enhanced stress resistance and protection against Aβ and polyQ40 proteotoxicity, AD and Huntington’s disease-associated proteins, respectively (El-Ami et al., 2014). This evidence concerns the gene IGF1R and Alzheimer disease.