Loss of response to Fas in HCC may be produced either by downregulation of Fas expression [14, 15], concomitant with decreased expression of downstream molecules, such as FADD or caspase-8 (also known as FLICE) [15], or by upregulation or overactivation of molecules that counteract its pro-apoptotic effect, including nuclear factor-kappa B (NF-κB), Bcl-2 or Bcl-XL [16–18]. Here, BCL2L1 is linked to hepatocellular carcinoma.