The transient silencing of ANRIL/CDKN2B-AS1 triggered an increase in INK4A/CDKN2A and INK4B/CDKN2B expression and impaired the metastatic ability of CM and UM cells in vitro; also, tumor formation induced by UM cells was inhibited both in vitro and in vivo by lncRNA knockdown [275]. Here, CDKN2B is linked to neoplasm.