Huang et al. demonstrated that TUG1 was activated by the nuclear transcription factor SP1 in HCC, and upregulation of TUG1 could inhibit the tumor-suppressor gene Kruppel-like factor 2 (KLF2) via binding to polycomb repressive complex 2 (PRC2) and recruiting it to KLF2 promoter region [22]. Here, KLF2 is linked to neoplasm.