These observations, taken together with the enhanced activation of STAT3 and AKT signaling shown in Figure 2, aligns with growing evidence that LPS-mediated TLR4 activation promotes chemo-resistance in cancer [51,52] by engaging pro-survival and anti-apoptotic pathways (particularly the AKT/NF-κB/STAT3 cascades) [51,53], thereby diminishing the cytotoxic effectiveness of chemotherapeutic agents such as doxorubicin. The gene discussed is AKT1; the disease is cancer.