Studies in model animal systems that delete or overexpress the "Alox5" gene have given seemingly paradoxical results. In mice, for example, Alox5 overexpression may decrease the damage caused by some types yet increase the damage caused by other types of invasive pathogens. This may be a reflection of the array of metabolites made by the Alox5 enzyme some of which possess opposing activities like the pro-inflammatory chemotactic factors and the anti-inflammatory specialized pro-resolving mediators. Alox5 and presumably human ALOX5 functions may vary widely depending on the agents stimulating their and types of metabolites they form; the specific tissues responding to these agents; the times (e.g. early versus delayed) at which observations are made; and, very likely, various other factors.