Co-expression of Rac1b in colonocytes counteracts B-RAF-induced senescence, expression of SA-β-gal, p14ARF, p15INK4B and p21WAF1 (which are all regulated by TGF-β), and suppression of proliferation marker Ki67 [22], indicating the selection for increased Rac1b expression as one potential mechanism by which tumor cells can escape from B-RAF-induced senescence. Here, CDKN2B is linked to neoplasm.