In this investigation of combination treatment with doxorubicin and three doses of FO/Se in a mouse model, we observed that FO/Se increased the inhibitory effects of doxorubicin on the receptor tyrosine kinases EGFR and FGFR and increased its therapeutic targeting of downstream signaling pathways (PI3K/Akt/mTOR, Ras/MEK/ ERK, and JAK2/Src-1/STAT3) involved in tumor PD-1/PD-L1 immune regulation, cancer stemness, angiogenesis, and tumor growth, as shown in Figure 7. The gene discussed is AKT1; the disease is neoplasm.