Furthermore, if decursinol-induced ataxia was solely responsible for the attenuation of nociceptive behaviors, it is unlikely that decursinol or other related AGN-derived compounds would affect inflammatory processes: inhibiting levels of pro-inflammatory cytokines (TNF-α and IL-1β; Kim et al., 2006; 2010; Ma et al., 2009) while simultaneously increasing levels of anti-inflammatory cytokines (IL-4 and IL-13; Lee et al., 2020). The gene discussed is IL4; the disease is Ataxia.