Prader–Willi syndrome (PWS) is a rare and complex genetically determined neurodevelopmental disorder. PWS. It is caused by the loss of function of paternal genes in a particular region of chromosome 15q11.2-q13. It is the most common genetic cause of life-threatening obesity in humans. It occurs in 1 in 15,000 to 1 in 30,000 infants, and both sexes are affected equally. PWS is characterized by severe hypotonia and feeding difficulties in early infancy, followed by excessive eating and gradual development of morbid obesity in early childhood, together with a series of comorbidities including short stature, typical facial dysmorphism, psychomotor delay, behavioral abnormalities, and cognitive impairment. Obesity is the reason why this syndrome is related to many difficulties. When PWS was discovered, a child with PWS had small or no chance for survival. Today, the PWS diagnosis can be confirmed as early as in the first month of life using DNA testing (analysis). The cure for PWS is still not found; however, some medications and procedures can reduce the incidence of physical symptoms of the disease and significantly improve the quality of life. Up to date, several kinds of treatment have been used, such as growth hormone therapy, nutritive measures, sex hormone replacement, thyroid hormone replacement, and promotion of psychomotor development. Although no drugs have proven effective in controlling appetite and weight gain in PWS, there are reasons to be hopeful. Many anti-obesity medicines and other therapeutic modalities currently in clinical development, described in this paper, can offer new therapeutic options for individuals with PWS. The most promising results were noted in treatment with neuropeptide oxytocin, its analog carbetocin, and Indian cactus succulent Caralluma fimbriata extract (CFE). With early diagnosis and improved new treatment, the quality of life of individuals with PWS can be improved, severe health complications prevented, and life expectancy prolonged.