Therefore, DNMT inhibitors are expected to show a beneficial impact to attenuate the effects of DNA hypermethylation on CDKN2A, PPARG, FAS, and PYCARD. In contrast, DNA hypomethylation in TWIST1 is involved in the development of CTCL, suggesting that DNA methylation-targeted treatment might have difficulty regulating both hypomethylation and hypermethylation of DNA by chemical agents and could be a reason for the limited number of studies regarding the efficacy of DNMT inhibitors against CTCL. This evidence concerns the gene PYCARD and primary cutaneous T-cell non-Hodgkin lymphoma.