In this report, ARHI has been re-expressed at physiologic levels,16 and an earlier study from our group found that overexpression of ARHI by infection of SKOv3 ovarian cancer cells and MDA-MB-231 breast cancer cells with ARHI adenovirus induced apoptosis through a caspase-independent, calpain-dependent mechanism.36 Recently, Li et al.37 also reported that overexpression of ARHI in TOV12D and ES2 ovarian cancer cells induced apoptosis and autophagic cell death by inhibiting activity of AKT and decreasing the expression of Bcl-2. This evidence concerns the gene AKT1 and breast carcinoma.