HAP1 and triple-negative breast carcinoma: The discrepancies between our primary study in human HAP1 and MelJuSo cell lines and mouse knock out system likely relate to differences in the cell type rather the strategy to knock out C9orf82. We like to note, that our initial functional analysis of C9orf82 inactivation was limited to the characterization of the HAP1 C9orf82 ko clone whereas our analysis of triple negative breast cancer patients failed to reveal any correlation between C9orf82 protein expression and the response to the treatment with doxorubicin-containing regimen [11].