The chromosomal constitution of a mammosomatotrophic and an inactive transplantable pituitary tumor induced in rats by 2,4,6-trimethylaniline was studied by the Giemsa-banding techniques. The inactive tumor line 7315i evolved from the active tumor line 7315a in one of the early transfers. A comparison was also made with chromosomal patterns of a transplantable rat hepatoma (7316A) induced by the same chemical carcinogen. Pituitary tumor line 7315a had a pseudotriploid complement with 63 chromosomes, whereas the inactive line 7315i was hypodiploid, with a dominant stemline of 36 chromosomes. The stemline chromosome number of the hepatoma was in the hypotetraploid region. Giemsa banding revealed that all chromosomes of the normal rat complement were present in both pituitary tumors. Four abnormal chromosomes were detected in the active tumor line and three in the inactive line. Both tumor lines contained a single minute chromosome. One common marker, a deleted chromosome No.1, was found in both pituitary tumors. This common marker chromosome was, however, not present in the hepatoma. The stemline karyotype of the hepatoma contained seven different markers, but none of them was identical to the abnormal chromosomes of the pituitary neoplasms. The findings suggested that the abnormal karyotypes of lines 7315a and 7315i could reflect the multisecretory activities of these neoplastic pituitary cells but that chromosomal localization of the secretory defect awaits exact genetic mapping of the rat chromosomes.