These findings are in line with previous ones showing that overexpression of HIPK2 suppresses the expression levels of proinflammatory TNF-α and IL-1β proinflammatory cytokines in spinal cord-injured rats [90] and attenuates sepsis-mediated liver injury [91] and that, in cancer cells, HIPK2 can block the inflammatory phenotype induced by VEGF/PGE2 production [45,69], underlining an important role for HIPK2 in suppressing inflammation-induced tumor progression. Here, VEGFA is linked to neoplasm.