Our specific aim was to demonstrate that (1) ERF is a suitable drug candidate for the treatment of CTCL, but the transcription factor TWIST 1 reduces the efficacy of ERF in TWIST1 expressing CTCL cell lines, and (2) combining ERF with MCRM will increase the antineoplastic effect of both substances, thus leading to a significant TWIST1 inhibition, deactivation of PKB/Akt and NF-κB, and suppression of Staphylococcus aureus biofilm formation. The gene discussed is ERF; the disease is primary cutaneous T-cell non-Hodgkin lymphoma.