Yet, based on the finding that the Arg117Gly mutant expressed no intrinsic activity, but readily dimerized to the wild-type protein without abolishing its activity, we hypothesize that this mutation and, probably, other yet unidentified CHEK2 mutations with a similar lack of intrinsic kinase activity, may cause resistance to anthracycline therapy if combined with LOH in breast cancer. Here, CHEK2 is linked to breast cancer.