Previous animal studies have also reported that normal ranges of hormone substitution restored CaMKII, calmodulin, SNAP-25 and neurogranin but not protein kinase C-γ and syt-1 in hypothyroid rats (1,13), indicating that T4 replacement therapy causes asynchronous recovery of adult-onset hypothyroidism-induced molecular impairments in the brain. The gene discussed is CAMK2G; the disease is hypothyroidism.