We speculated that a genetic ablation or downregulation of JunB or the proteinous-functional dysregulation of JunB may contribute to an unfavorable elevation of S100A8/A9 and probably of other soluble inflammatory factors that would function together in a complex manner to directly activate cancer cells themselves and to provide a suitable site for cancer cells to transition toward more aggressive phenotype. The gene discussed is JUNB; the disease is cancer.