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Cover p27 functions as an oncogene in a CDK-independent manner. Shown here is an immunofluorescence analysis of a lung from a mouse homozygous for p27CK−, a knock-in mutant allele of p27KIP1. The p27CK− protein contains four amino acid substitutions that prevent its binding to cyclins and CDKs. Unlike p27-null mice, p27CK− mice display a high incidence of spontaneous tumorigenesis in multiple tissues, including the lung. The tissue was stained with DAPI (blue), as well as antibodies directed against an alveolar epithelial protein (Surfactant protein-C; red) and a bronchiolar epithelial protein (Clara Cell-Specific Protein; green). Cells simultaneously expressing both bronchiolar and alveolar markers are typical of bronchioalveolar stem cells (BASCs), and are abundantly and abnormally present throughout the dysplastic p27CK− bronchiolar epithelium. (For details, see Besson et al., p. 1731.)