RB1 and cancer: 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).