The same treatments also induce reduction of the permissive mark H3K4me3 at P16INK4a , an important tumor suppressor gene whose silencing plays a pivotal role in photo carcinogenesis [138,139], accompanied by a substantial increase of its promoter DNA methylation, leading to a drastic decrease of the P16INK4a mRNA expression with 20-fold (for 10 weeks) and 40-fold (for 15 weeks) [140]. Here, CDKN2A is linked to neoplasm.