The association between chronic inflammation and lung cancer has been extensively reported. Despite the differences in the clinical manifestations of chronic obstructive pulmonary disease (COPD) compared with lung cancer, the underlying inflammatory pathogenesis of these two diseases may involve shared biological features. Identifying the mechanisms that regulate specific inflammatory mediators shared by both diseases will represent a major breakthrough. Chemokines play an important role in the inflammatory response. Recent evidence suggests that post-transcriptional regulation, through control of mRNA stability, could be an important mechanism of regulation of chemokine expression. Therefore, it would be important to study the role of RNA-binding proteins, such as hnRNPs, in chemokine expression after initial inflammatory response. HnRNPs have shown the ability to modulate inflammatory mediators expression by affecting mRNA stability of COX-2, TNFalpha and IL-1beta and iNOS. Moreover, overexpression of hnRNPs has been reported in cancer, for example, hnRNP A2/B1 in lung cancer. Thus, investigating the role of hnRNPs in chemokine expression may allow us to understand the molecular mechanisms involved in the regulation of the inflammatory response before its progression to chronic inflammation and/or tumor development.