Importantly, increased MCL-1 protein levels through PI3K/AKT signaling can enhance MCL-1 pro-survival functionality in the absence of genomic and transcriptomic MCL1 upregulation, indicating that targeting mTOR-mediated MCL-1 translation may provide an additional mechanism by which MCL-1 protein levels can be suppressed in some breast cancer subtypes (Figure 3) [71]. This evidence concerns the gene PIK3CA and breast carcinoma.