p56lck activity increased Id3 transcript levels in cultured lymphocytes [32], and cell lines derived from lymphomas arising in mice overexpressing p56lck [33] provided a system to assay Id3-mediated repression of p27. Cells were treated with a pharmacologic inhibitor highly specific for src-family protein tyrosine kinases, PP1 [34]. This evidence concerns the gene CDKN1B and lymphoma.