Additionally, several gene mutations, including fumarate hydratase (cAMP and PKA pathway inhibition), MEN1 (menin-induced inhibition of several tumor suppressor pathways), APC (Wnt/β-catenin signaling stimulation, GIP, 5-HT7, and abnormal LH receptor expression), GNAS (GNAS/PKA/CREB activation), EDNRA (MAPK signaling activation), L205R in PRKACA (PKA pathway activation), MC2R (MC2R/PKA/CREB activation), and PDE8B and PDE11A (cAMP hydrolysis and PKA pathway inhibition), inhibit tumor suppression and enhance steroidogenesis [74,75,76,77,78,79,80,81,82,83]. The gene discussed is GNAS; the disease is neoplasm.