On 2014 Jul 25, Jens Staal commented:

The VRPR experiment was unfortunately not the best verification that we could have done. In a later experiment, we silenced the uncleavable CYLD in our stable Jurkat cells with siRNA and could restore JNK activation to levels equal to that of normal Jurkats silenced for CYLD, providing further proof that the uncleavable CYLD is indeed causing the JNK inhibition and that it is not a clonal effect.

On the other hand, later results indicate that MALT1 protease activity is not required for JNK activation so the most likely explanation for our observations is that they are visible thanks to the overexpression of CYLD (both WT and R/A are overexpressed to the same extent so the difference is cleavage-dependent) whereas the effect is not visible when expressed at endogenous levels.

On 2014 Jul 25, Jens Staal commented:

The VRPR experiment was unfortunately not the best verification that we could have done. In a later experiment, we silenced the uncleavable CYLD in our stable Jurkat cells with siRNA and could restore JNK activation to levels equal to that of normal Jurkats silenced for CYLD, providing further proof that the uncleavable CYLD is indeed causing the JNK inhibition and that it is not a clonal effect.

On the other hand, later results indicate that MALT1 protease activity is not required for JNK activation so the most likely explanation for our observations is that they are visible thanks to the overexpression of CYLD (both WT and R/A are overexpressed to the same extent so the difference is cleavage-dependent) whereas the effect is not visible when expressed at endogenous levels.