Notably, KLF4 has been demonstrated to induce cancer stem cell-like phenotypes in nonstem cancer cells,27 whereas CEBPG has been implicated in promoting disease progression across various cancers.28–30 Conversely, TFs silenced in resistant cells, such as CEBPD and NR1H4, play critical roles in promoting immune and inflammatory gene expression while enhancing tumor cell chemosensitivity31–33 (Supplementary Fig. 11 and Supplementary Data 6). The gene discussed is CEBPG; the disease is neoplasm.