In comparison, TEP6 inactivation decreases PO and melanization in flies following infection, but exhibits lesser susceptibility to bacteria[26]. Further mechanistic studies showed that TEP4 inactivation upregulates the Toll and immune deficiency (IMD) signaling pathways while downregulating the Janus kinase(JAK)/signal transducer and activator of transcription (STAT) and c-Jun N terminal kinase (JNK) pathways upon infection [29]. TEP2 mutants, which do not affect Toll pathway activation but reduce IMD pathway activity, suggest that TEP2 and TEP4 operate through different mechanisms [30]. This evidence concerns the gene SOAT1 and infection.