It is expected that MAPK-dependent recombinant vaccinia virus (MDRVV) with deletions in both VGF and O1 would be more highly attenuated in normal cells and could replicate in tumor cells that exhibit constitutive ERK1/2 activation in the MAPK pathway due to oncogenic mutations in the EGFR, RAS, and Raf genes [24,25,26]. The gene discussed is VGF; the disease is neoplasm.