Generally, the underlying mechanisms in humoral hypercalcaemia of malignancy are associated with PTHrP (PTHLH) over-secretion as described in CCAs which might act as growth promotor via activation of the ERK (extracellular signal-related kinase)–JNK (c-Jun N-terminal kinase)-ATF2 (activating transcription factor-2)-cyclinD1 pathway (this canonical path explains the paracrine effects of PTHrP) [173]. The gene discussed is ATF2; the disease is Hypercalcemia.