Using this, we observed that in fetal cortices exposed to CAI in utero, as well as in various cell systems exposed to alcohol ex vivo (including F9 embryonic carcinoma cells, in which, as in the developing cortex, HSF2 displays high constitutive DNA-binding activity, but HSF1 does not; Rallu et al, 1997; Supplementary Fig S8), both HSF1 and HSF2 were activated, as assessed by the virtually complete supershifting of the HSF–HSE complex by either anti-HSF1 or anti-HSF2 antibodies in gel-shift. The gene discussed is HSF1; the disease is embryonal carcinoma.