Several cellular pathways that are currently known to contribute to MYXV's ability of MYXV to replicate in human cancer cells include (i) endogenously activated protein kinase B (PKB)/AKT, (ii) antiviral pathway activated by protein kinase R, (iii) status of tumor suppressors such as p53, Rb, and ataxia telangiectasia, and (iv) antiviral states induced by IFNs or TNF (16–19). This evidence concerns the gene AKT1 and cancer.