The centrality of PKR inhibition by the RAS/RAF/MEK/ERK signaling axis in determining susceptibility of cancer cells to OVs is further exemplified by: (i) the requirements of herpes simplex virus 1 (HSV1) Δγ(1)34.5 mutants for MEK-mediated PKR inhibition [44], (ii) the oncotropism of VAI mutant adenovirus towards cells in which RAS inactivates PKR [45], and (iii) the selectivity of the mammalian reovirus towards RAS-transformed cells, which was initially identified as dependent on PKR inactivation [46,47]. This evidence concerns the gene EIF2AK2 and cancer.