The phenotypes werecorroborated with whole larvae imaging, showing lower bacterial foci in RΔeccC3, as compared to the parental R strain.Moreover, infection with R ΔeccC3 was associatedwith a lower pro-inflammatory response, as showcased by the reducedproduction of il1b and tnfa transcripts.Together, these findings demonstrate that ESX-3 is a primary driver ofMab R pathogenicity. The gene discussed is TNF; the disease is infection.