hTERT is reactivated in the majority of cancer patients. Methylation on hTERT promoter is the 1st rank cause on the list of upregulation hTERT expression based on the investigation result of thousands of cancer patients. The inspection mechanism of hTERT promoter methylation in cancer patients is very guidance for a better understanding of telomerase reactivation in cancer. The authors examined the hTERT promoter methylation profiles in individual SS patients and patient-derived cells. The results revealed the higher methylation level on the THOR region of hTERT promoter in all tested CTCL related samples, including CTCL cell lines, SS patients, and their derived cells. The further study results demonstrated that methylation regulation on the THOR region is independent of WT1, a repressor for hTERT expression, and histone modification in SS patients. Although the deep mechanism underlying the methylation status in CTCL still need to be studied more, the results in the manuscript provide a potential hallmark in SS patients.

My comments are the following:
1. In the fig 5A, hTERT promoter activity was repressed with WT1 overexpression. However, since expression from transit transfection hTERT-Luc vector is independent of chromatin restriction in cells, the experiment result didn’t represent the real hTERT promoter activity in cells. Checking the hTERT mRNA expression with WT1 overexpression is more reliable for demonstrating the relationship between hTERT and WT1.
2. In the fig5B, the authors didn’t detect the binding signal of WT1 on the target site TERT-323. However, this result might be caused by the inefficiency amplification by PCR primers since no positive control on this site. Secondary, the PCR fragment for TERT-323, which was amplified by the PCR primers in table S2, didn’t include the WT1 binding site. Additionally, the authors normalized the data with genomic DNA. Usually, the ChIP-PCR data was normalized with input or IgG ChIP data.
3. In the figS3, the WT1 protein expression (B) in samples is not consistent with mRNA expression (A). It is better if the authors could provide protein expression statistic data.

In the revised manuscript, the authors have addressed most of the concerns raised previously.
To provide readers of the journal with a more concise interpretation of the results, please address the following points:
1. The result of supplementary figure 5 well-supported figure 5A. To address the point more clearly, I suggested presenting these figures together in figure 5.
2. I recommend adding the reference in the method for interpreting how to analyze qRT-PCR data.