As not only cell cycle inhibitors p16 and p19 are controlled by CTCF, but also c-Myc (Lobanenkov et al., 1990; Gombert and Krumm, 2009), pRb (De La Rosa-Velazquez et al., 2007), p21 and p27 (Qi et al., 2003), loss of CTCF function may support cancer formation and indeed, 87.7% of tested breast tumors showed alterations in the ratio between PARylated 180 kDa and 130 kDa forms of CTCF. The gene discussed is CDKN2A; the disease is cancer.