Missense mutations or in-frame deletions near S33, S37, T41, and S45 in β-catenin lead to functionally acquired β-catenin mutants that are resistant to ubiquitin-mediated proteasome degradation and induce the upregulation of oncogenic target genes such as CCND1 and MYC in tumors, including lung cancer. This evidence concerns the gene CCND1 and lung cancer.