Recently attempts have been made to demonstrate the possible role of hypergastrinemia in the production of congenital hypertrophic pyloric stenosis in infants. Eleven infants with congenital hypertrophic pyloric stenosis, ranging in age from three to 11 weeks, were evaluated for fasting and postprandial serum gastrin levels. Two to ten weeks following successful pyloromyotomy, a similar evaluation was undertaken to demonstrate the possible role of elevated serum gastrin levels in the etiology of congenital hypertrophic pyloric stenosis. The average fasting and postprandial serum gastrin levels in infants with congenital hypertrophic pyloric stenosis did not differ significantly from levels noted in control infants. Similarly, no statistically significant difference was noted between the pre- and postoperative levels of serum gastrin in the affected infants. Several experimental studies have been reported within the past few years describing the production of hypertrophic pyloric stenosis in the offspring of dogs injected with pentagastrin during pregnancy. The results of our study minimize the direct importance of serum gastrin in the production of congenital hypertrophic pyloric stenosis. The role of the hormone secretin in the etiology of this condition is hypothesized.