CDKN2A and neoplasm: In the last few years, many studies have investigated the molecular steps behind the development and progression of CTCL, which includes recurrent deletions of tumor suppressors (e.g., ARID1A, CDKN2A/B, PTPRC, SOCS1, and STK11), gene mutations of PLCG1 and JAK3, and epigenetic alterations such as histone/chromatin modifications and hypermethylation of multiple tumor suppressor genes (e.g., BCL7a and CDKN2A/B).