As shown in Figure 1A, the C. elegans glp-4;sek-1 double mutant was significantly more susceptible to Candida than the glp-4 mutant (p < 0.001), suggesting that the C. elegans homolog of the mammalian p38 mitogen-activated protein kinase (which is involved in mammalian response to candidiasis [12]) plays a significant role in the C. elegans response to Candida. This finding is consistent with the observation that sek-1 mutants are more susceptible to a variety of pathogens [7,11]. This evidence concerns the gene MAP2K4 and candidiasis.