On the one hand, Li et al. demonstrated that miR-223-3p modulates the noncanonical NF-κB (nuclear factor-κB) pathway by targeting transcripts of the inhibitor of kappa B kinase alpha (IKKα) (engaged in activation of NF-κB), which is an anti-inflammatory factor that may prevent the spontaneous activation of macrophages, thus promoting controlled inflammation in the human myeloid leukemia cell line [154]. This evidence concerns the gene NFKB1 and myeloid leukemia.