We suggest three possible mechanisms for the observed co-regulatory pattern of the TNFAIP1/POLDIP2 SFGM: an amplification mechanism (recurrent amplification), - if the modules are located in an amplified region on 17q involved in the process of breast cancer development; a chromatin remodeling/activation mechanism (for example, histone modification); and a transcription activation mechanism (for example, common regulatory transcription factors). The gene discussed is POLDIP2; the disease is breast cancer.