In hyperparathyroidism, the receptor activator of the nuclear factor kappa B ligand (RANKL) was shown to be hyperexpressed and, as a consequence, to be responsible for the catabolic effect of PTH (1–34) in bone.(41, 42) RANKL is involved in the major pathways utilized in PTH‐induced resorption: the Rankl/Rank/Opg system. The gene discussed is PTH; the disease is hyperparathyroidism.