Further, as the treatment of fibroblast cells derived from FXS patients, with small molecules that block S6K1 and phosphoinositide 3-kinase (PI3K) catalytic subunit p110β, decreased the rates of protein synthesis in both control and patient fibroblasts; the role of these targets as a potential biomarker should be considered [111]. The gene discussed is PIK3CD; the disease is fragile X syndrome.