KLF4, a zinc finger transcription factor with context-dependent roles in cancer, is predominantly tumor-suppressive in HCC, where its low expression correlates with poor differentiation, unfavorable prognosis, and worse outcomes after liver transplantation.56, 57 Functionally, it suppresses HCC progression by inhibiting EMT through downregulation of Slug (SNAI2),58, 59 suppressing EGFR and JNK signaling, reduces migration through inducing P-cadherin.60 Here, CDH3 is linked to neoplasm.