NFATC1 and neoplasm: Here, we consistently showed that the presence of RANKL and M-CSF markedly evoked the expressions of TRAF6, BRD4, and NFATc1, the degradation of IκB-α, the reduced cytosolic p65, and the increased nuclear p65 in blood mononuclear cells from either normal or tumor group, indicating RANKL and M-CSF induced the activation of RANKL-NF-κB signal pathway (Figure 2A,B).