This condition is usually caused by mutations in the FAS gene.

This finding suggests that the Fas gene is involved in the signalling mechanism that normally causes the self-reactive white blood cells to die.

In humans it is transcribed from the opposite strand of intron 1 of the FAS gene.

Because deletions of some fas genes give a non-virulent phenotype, for fas a main role in virulence was proposed .

Lieberman's lab recently demonstrated the ability of RNAi to silence expression of the Fas gene in mice, protecting them from fulminant hepatitis.

It has been shown that Butyrate inhibits activity of HDAC1 that is bound to the Fas gene promoter in T cells, resulting in hyperacetylation of the Fas promoter and up-regulation of Fas receptor on the T cell surface.