The study investigates the senescence-like cell cycle arrest of human naevi, which are benign tumors of melanocytes often carrying oncogenic mutations in the BRAF gene. The research shows that sustained expression of the BRAF^V600E mutation in human melanocytes leads to cell cycle arrest, accompanied by the induction of p16^INK4a and senescence-associated acidic β-galactosidase (SA-β-Gal) activity. This senescence is validated in vivo, as congenital naevi consistently exhibit SA-β-Gal activity, a marker of senescence. The study also finds that the p16^INK4a protein is upregulated in response to BRAF^V600E expression but is not strictly required for the induction of cell cycle arrest. Additionally, the research suggests that telomere attrition is not a major factor in the senescence of naevi, as telomere lengths are similar in congenital and acquired naevi. These findings support the hypothesis that oncogene-induced senescence is a physiological process that limits the progression of premalignant lesions.The study investigates the senescence-like cell cycle arrest of human naevi, which are benign tumors of melanocytes often carrying oncogenic mutations in the BRAF gene. The research shows that sustained expression of the BRAF^V600E mutation in human melanocytes leads to cell cycle arrest, accompanied by the induction of p16^INK4a and senescence-associated acidic β-galactosidase (SA-β-Gal) activity. This senescence is validated in vivo, as congenital naevi consistently exhibit SA-β-Gal activity, a marker of senescence. The study also finds that the p16^INK4a protein is upregulated in response to BRAF^V600E expression but is not strictly required for the induction of cell cycle arrest. Additionally, the research suggests that telomere attrition is not a major factor in the senescence of naevi, as telomere lengths are similar in congenital and acquired naevi. These findings support the hypothesis that oncogene-induced senescence is a physiological process that limits the progression of premalignant lesions.