Additionally, it has been reported that overexpression of β-catenin, a coactivator of LEF1, results in p53 accumulation through upregulation of ARF [41,42] and the N-terminal of LEF1 (ΔNLef1), which acts as a tumor promoter by preventing accumulation of p53 in human and mouse sebaceous tumors, and ARF downregulation is likely to be responsible for this mechanism [43]. This evidence concerns the gene LEF1 and neoplasm.