Our work demonstrates that while CDK8 binding is altered in leiomyoma tissue samples, characterized by both a loss of binding affinity at a subset of sites and a recruitment of CDK8 at new sites, the observed change is not consistent with a global loss of CDK8 recruitment that would result from a mutation-dependent MED12-cyclin C-CDK8 interaction defect. Here, CDK8 is linked to leiomyoma.