CTR1 is related to a greater influx of CIS into the cells; our results indicated that there is a balance between the expression of ATP7A/B and CTR1. Furthermore, the downregulation of ATP7A/B genes observed in SiHaCIS-R cells treated with PTX may contribute to the sensitization of cells that are resistant to CIS, due to that PTX alone or in combination with CIS induced DNA fragmentation and caspase activity, as well as the decrease in the phosphorylation of p65 and in anti-apoptotic proteins (Blc-2 and Bcl-XL). The gene discussed is ATP7A; the disease is in situ carcinoma.