AMCase is induced during TH2 inflammation through an interleukin (IL)-13 dependent mechanism and has been demonstrated to be heavily over-expressed in human asthmatic tissue [10,12]. Inhibition of the AMCase with the well known chitinase inhibitor allosamidin reduced the inflammation [12]. The fact that chitinases are a factor in host antiparasite responses and in asthmatic TH2 inflammation led to the hypothesis that asthma may be a parasite-independent antiparasite response [10], which again suggests that inhibition of AMCase is a potential target for asthma therapy [9–12]. It has been shown that partially deacetylated CHOS can function as inhibitors of family 18 chitinases [103–105]. There is therefore a great potential for CHOS as an anti-inflammatory drug in patients with asthma. For a more detailed description of this and related topics, see the review by Muzzarelli in this special issue of Marine Drugs [143].