 PRC1, PRC2, YY1, and Id1 play a role in the suppression of p16INK4A expression and transcription factors CTCF, Sp1, and ETs activate p16INK4A transcription.In knockout experiments, it was found that mice lacking just p16INK4a were more prone to spontaneous cancers.Mice lacking both p16INK4a and ARF were found to be even more tumor prone than the mice lacking just p16INK4a.