Similarly, in humans, some gain-of-function Gα11 mutations result in autosomal dominant hypocalcaemia (ADH) type-2 while some loss-of-function Gα11 mutations produce a familial hypocalciuric hypercalcemia (FHH)-like condition (Nesbit et al., 2013). This evidence concerns the gene GNA11 and familial hypocalciuric hypercalcemia.