You will be shown a scientific claim, and the abstract of a biomedical research paper. Each sentence from the abstract will be on a separate line. Your task is to return a JSON object with two fields:

- "verdict": The fact-checking verdict. If the information in the abstract supports the claim, write "SUPPORT". If the abstract contradicts the claim, write "CONTRADICT". If the abstract does not provide enough information to arrive at a verdict, write "NEI" (for "not enough information").
- "evidence": An array of sentences providing evidence for the verdict. Please copy all relevant sentences verbatim from the abstract. If the verdict was "NEI", then return an empty array.

For instance, if the model were given the claim "smoking causes cancer", the output might be
{
  "verdict": "SUPPORT",
  "evidence": ["The results of our meta-analysis provide overwhelming support that cigarette smoking is a risk cause for lung cancer."]
}

Your response should not include any text other than the json.

Claim: The G34R/V mutation does not create a hypomethylated phenotype at the H3K36 histone.

Abstract:
Recognition of modified histones by ‘reader’ proteins plays a critical role in the regulation of chromatin.
H3K36 trimethylation (H3K36me3) is deposited onto the nucleosomes in the transcribed regions after RNA polymerase II elongation.
In yeast, this mark in turn recruits epigenetic regulators to reset the chromatin to a relatively repressive state, thus suppressing cryptic transcription.
However, much less is known about the role of H3K36me3 in transcription regulation in mammals.
This is further complicated by the transcription-coupled incorporation of the histone variant H3.3 in gene bodies.
Here we show that the candidate tumour suppressor ZMYND11 specifically recognizes H3K36me3 on H3.3 (H3.3K36me3) and regulates RNA polymerase II elongation.
Structural studies show that in addition to the trimethyl-lysine binding by an aromatic cage within the PWWP domain, the H3.3-dependent recognition is mediated by the encapsulation of the H3.3-specific ‘Ser 31’ residue in a composite pocket formed by the tandem bromo–PWWP domains of ZMYND11.
Chromatin immunoprecipitation followed by sequencing shows a genome-wide co-localization of ZMYND11 with H3K36me3 and H3.3 in gene bodies, and its occupancy requires the pre-deposition of H3.3K36me3.
Although ZMYND11 is associated with highly expressed genes, it functions as an unconventional transcription co-repressor by modulating RNA polymerase II at the elongation stage.
ZMYND11 is critical for the repression of a transcriptional program that is essential for tumour cell growth; low expression levels of ZMYND11 in breast cancer patients correlate with worse prognosis.
Consistently, overexpression of ZMYND11 suppresses cancer cell growth in vitro and tumour formation in mice.
Together, this study identifies ZMYND11 as an H3.3-specific reader of H3K36me3 that links the histone-variant-mediated transcription elongation control to tumour suppression.
{"verdict": "NEI", "evidence": []}