BAX and cancer: In agreement with literature, demonstrating that an imbalance of the Bax/Bcl2 ratio in favor of Bcl2 contributes to rendering cancer cells more resistant to apoptosis36, HTLA-ER cells, after short-term etoposide exposure, show an increased amount of Bcl2 that efficiently counteracts the pro-apoptotic function of BAX and/or PUMA (Figs 1 and 2 supplementary)37 becoming unable to undergo apoptosis (Fig. 7).