A parsimonious explanation as to why no opposing regulatory effects on pathogenesis were observed between the tar1Δ and gat1/are1Δ or double gat1/are1Δ tar1Δ mutants may relate to the scarce nutrient availability during in vivo infection, a condition in which Tar1 is predicted to positively regulate GAT1/ARE1 activity [34]. Here, VPS52 is linked to infection.