The search for compounds capable of modulating the actions of HSF1 is already a focus for therapeutic strategies for cancer and neurodegenerative diseases (Westerheide & Morimoto, 2005; Whitesell & Lindquist, 2009; Neef et al, 2010, 2011), and it is tempting to consider our findings of the essential role of HSF2 in the fetal cortex as a basis for strategies to prevent or limit brain damage in the case of FAS. This evidence concerns the gene FAS and cancer.