Specifically, the levels of dsRNA were found to be increased in a chicken model and in patients with osteomyelitis, and DICER1 (encoding endoribonuclease for dsRNA cleavage) knockdown or Staphylococcus infection-induced dsRNA accumulation upregulates IL-1β and IL-18 expression in and reduces viability of human osteoblasts via activation of the NLRP3 inflammasome, indicating that DICER1 and dsRNA dysmetabolism is an upstream regulator of NLRP3 signaling in infected osteoblasts as a model of osteomyelitis (311). This evidence concerns the gene DICER1 and staphylococcus aureus infection.