CHEK1 and breast cancer: In addition, the data shown here disclose a new mechanism through which BC cells control ERα stability and abundance via CHK1 activity and further demonstrate that targeting ERα-positive cells modeling primary and MBC with clinically relevant CHK1 inhibitors alone or in combination with ET drugs (i.e., Tam) or with drugs used for the treatment of MBC (i.e., Abe and Palbo) represent an appealing strategy to prevent ERα-positive BC cell proliferation.