The early activations of JNK and ERK were important for early cytokine/chemokine responses towards the infection, which was demonstrated by the wide spread inhibition of inflammatory mediators including TNFα, IL-6, MCP-1, MIP-1α/CCL3, RANTES/CCL5, KC/CXCL1, IP10/CXCL10, and G-CSF upon inhibition of JNK and/or ERK alone [49]. The gene discussed is CXCL10; the disease is infection.