In line with studies underlying the crucial role of NF-κB in the survival and activation of monocytes [19], NF-κΒ pathway inhibitors, such as the compound “parthenolide” [20, 21], were predicted to reverse the SLE monocyte gene signature, whereas agents targeting the SLE-related Pim-1/NFATc1/NLRP3 signaling axis [22] might also represent promising therapeutic approaches. The gene discussed is PIM1; the disease is systemic lupus erythematosus.