In conclusion, our results suggest that mutations in GNAS, PDE4D, and PRKAR1A, and methylation changes in GNAS locus do not play a significant role in etiology of childhood-onset obesity in our Finnish cohort of patients, who lacked biochemical features of pseudohypoparathyroidism and related disorders. Here, PDE4D is linked to pseudohypoparathyroidism type 1A.