In comparison, PCM-susceptible mice (B10.A) induces an inadequate and disproportionate response by direct or indirectly downregulating several catabolic processes, essential for lysosomal function, and possibly to antigen presentation and the PPAR pathway, important in the modulation of inflammatory processes [70,71], while upregulating macrophage migration but not neutrophil or monocyte recruitment. This evidence concerns the gene PPARA and paracoccidioidomycosis.