We speculate that either (1) BRCA1 is rendered non-functional by some other mechanism (similar to p53); (2) it is functionally overwhelmed by genome instability over the long timescale of this cancer lineage, resulting in a similar phenotype to loss of function; and/or (3) a different pathway in bivalves is responsible for the tandem duplication phenotype; although we are unable to test these hypotheses in this study. Here, TP53 is linked to cancer.