Flatfoot syndrome can occur in children as well as in adults. The timing of surgical treatment for flatfoot deformity in children and the type of surgical treatment used remains a challenge. Symptomatic adult flatfoot is often referred to as adult acquired flatfoot disorder (AAFD), and posterior tibial tendon insufficiency (PTTD) is the most common cause of adult flatfoot disorder. Children with flat feet need to be examined to determine the extent of the deformity and be aware of any excessive joint laxity, which can cause corrective surgery to fail. Non-surgical treatment with corrective shoes and insoles is available for children. Commonly used surgical procedures include subtalar arthroplasty; paracarpal resection, posterior tibial tendon reconstruction; lateral column lengthening; and medial cuneiform open wedge osteotomy treatment. In recent years, many foot and ankle surgeons have used subtalar arthrodesis to treat children with flatfoot syndrome, and the results are significantly better than those for adults with flexible flatfoot syndrome. However, if the patient has a residual forefoot deformity after surgery, the forefoot will still be in a rotated posterior position. When the plantarflexion of the 1st metatarsal cannot compensate for such a change, there is still the potential for hindfoot valgus to cause pain in the subtalar joint, at which point an open wedge osteotomy of the medial cuneiform bone is required to correct the forefoot rotation posteriorly. The treatment of flatfoot syndrome in adults differs somewhat from that of children, and there are many different perspectives. Because there may be multiple satisfactory treatment modalities for the same deformity, trying to find a standardized approach is not only difficult, but also fraught with controversy. Physicians may be confused by the sheer number of options available to them when treating flatfoot syndrome. Flexibility or lack thereof of the hindfoot, or subtalar joint, is the focus of diagnosis and treatment of adult acquired flatfoot syndrome. Patients with mild deformity and no pain may be left untreated. Flexibility of the flatfoot is seen on examination with reduced strength of the posterior tibial tendon (rupture), heel exostosis, forefoot rotation back and abduction. After long-term follow-up, we believe that patients with stage II lesions with posterior tibial tendon rupture can be treated with internal displacement of the heel osteotomy and displacement of the long toe flexor tendon to the posterior tibial tendon. For rigid flatfoot syndrome, triple joint fusion combined with tendon transposition has definite efficacy. The balance of muscular forces is a prerequisite for fusion; if the forces between the tendons are not balanced, then the deformity may recur after fusion and the fusion is doomed to failure. In adults with stage IV acquired flatfoot with deltoid ligament rupture and degeneration of the soft tissues surrounding the ligament, conventional reparative surgery does not achieve sufficient strength. Often we can reconstruct the deltoid ligament using an autologous semitendinosus muscle to achieve adequate stability. Flatfoot syndrome is a complex deformity, and an individualized surgical treatment plan appropriate for the patient should be developed by examining the joint function of the patient’s foot in a posterior to anterior sequence. After correction of the deformity and restoration of foot stability, the treatment prognosis is still satisfactory.