RASSF4 regulates apoptosis through an environment-dependent dual mechanism; under stress or anti-cancer conditions (such as T-2 toxin exposure), its expression is activated by DNA demethylation and histone acetylation (H3K9ac), thereby promoting BCL2-associated X protein (BAX) activation and cytochrome C release and activating the caspase-9/3 cascade to induce apoptosis through the mitochondrial pathway [12,36]. Here, BAX is linked to cancer.