Reduced expression or null mutation of ORM1/2 specifically enhanced FLS2-dependent immune responses after infection by bacterial pathogen Pseudomonas syringae and increased the abundance of FLS2, while overexpression of ORMs caused FLS2 degradation and abrogated FLS2-dependent signaling, suggesting a broader role of ORM proteins beyond sphingolipid metabolic regulation (Yang et al., 2019). The gene discussed is ORM1; the disease is infection.