It is noteworthy that IL-6 and IL-36α expression are elevated following treatment with BPs.29 IL-6 subsequently activates the STAT3 pathway, while IL-36α activates the ERK signalling pathway and subsequently inhibits translocation of TGF-β1 and the Smad signalling pathway.21,29 Furthermore, TLR-4-mediated macrophage polarisation participates in the pathogenesis of BRONJ in mice.34 Therefore, it is possible that multiple signalling pathways participate in the pathogenesis of MRONJ. The gene discussed is IL36A; the disease is Bartsocas-Papas syndrome 1.