This is because the mutations in acrodysostosis (PRKAR1A or PDE4D) disrupt cAMP signaling downstream of the GNAS-encoded Gsα protein, leading to a broader and more severe impairment of the cAMP/protein kinase A (PKA) pathway in chondrocytes and osteoblasts, which are critical for endochondral bone formation and skeletal patterning [67,68]. This evidence concerns the gene PRKAR1A and acrodysostosis.