However, Sumbayev et al. [71], using human myeloid leukemia THP-1 cells exposed to the interleukin (IL) IL-1β, hypothesized that the anti-inflammatory activity of Au NPs may be attributed mainly to their extracellular interactions with IL-1β which aggregates around Au NPs, thus inhibiting IL-1β binding to cellular receptors. The gene discussed is IL1B; the disease is myeloid leukemia.