AbstractTwo recent reports of mice homozygously deleted for cyclin D1 provide unequivocal evidence that the critical G1cyclin, cyclin D1, is by itself rate‐limiting for growth in some mammalian tissues(1,2). Cyclin D1 knockout mice are small and exhibit behavioral abnormalities. Specific hypoplasias of retinal and mammary tissues suggest an unusual dependence on cyclin D1 function for tissue growth in those organs. The odd coincidences that cyclin D1 functions as the retinoblastoma gene kinase, together with associations between increased cyclin D1 expression and breast cancer, suggest, but do not prove, a special function of cyclin D1 in those tissue