Because CKS1B copy gain and increased expression in hypoxia were KDM4A-dependent, we hypothesized that hsa-mir-23a/b and hsa-mir-137 would promote gain and increased expression for CKS1B. To directly test this hypothesis, we transfected breast cancer cells (MDA-MB-231) with miRNA inhibitors for hsa-mir-23a, hsa-mir-23b, or hsa-mir-137 and assessed copy gain and gene expression. This evidence concerns the gene KDM4A and breast carcinoma.