In the absence of pathogens, BAK1 is constitutively sequestered by BIR2 (BAK1-INTERACTING RECEPTOR-LIKE KINASE 2) and BIR3 via physical interactions, which prevents spontaneous dimerization between BAK1 and FLS2, keeping FLS2-mediated immune responses inactive to avoid autoimmunity [57, 58]. The gene discussed is BAK1; the disease is Autoimmunity.