CCND1 and cancer: We speculate that during amplification events, duplicated genomic segments undergo the loss of their repressive epigenomic signatures, consequently enabling demethylation of MYEOV, and thereby leading to an overexpression of MYEOV RNA in cancer cells, and/or permitting the MYEOV-3′-putative enhancer to regulate CCND1, thereby boosting CCND1 expression.