KLF5 acts as a core regulator of intestinal oncogenesis, as demonstrated in a genetically manipulated mouse model that exhibits simultaneous oncogenic activation of Wnt/β-catenin signalling and KLF5 deletion, specifically in Lgr5+ intestinal stem cells.13 Overall, these findings suggest that KLF5 may be an appropriate target in a strategy to eradicate stem-like cells in CRC. The gene discussed is KLF5; the disease is colorectal carcinoma.