Herein, MERIT40 has been identified as substrate of Akt; Akt-mediated MERIT40 phosphorylation at S29 facilitated assembly of BRCA1 complexes in response to doxorubicin-induced DNA damage, execution of HRR and survival of doxorubicin-treated breast cancer cell lines (MCF7, SUM159 and T47D) independently of the Akt isoform and of mTORC1 [242]. This evidence concerns the gene BRCA1 and breast carcinoma.