Cell size, which differs markedly between species and cell types, has implications for cell physiology, growth and differentiation. However, the genetic control of cell size remains a long-standing enigma, particularly in multicellular organisms. We are studying this question in the Arabidopsis shoot apical meristem, where uniform cell sizes are maintained over extended periods of proliferation. Measurement of the sources of size variability, computer simulations and recovery from genetic perturbation indicated that meristem cell size is monitored and corrected. A key aim now is to reveal the molecular mechanism(s) of cell size homeostasis. Our recent data shows that after asymmetric cell division in the shoot meristem, the larger sister cell progresses more rapidly from G1 to S-phase. In unicellular organisms, size-dependent G1-S transition is controlled by components of the retinoblastoma (RB) pathway in Chlamydomonas or its functional equivalent (Whi5) in yeast. In our working model for the Arabidopsis shoot meristem, a component of the RB pathway associates with chromatin during mitosis and is distributed in equal amount to daughter cells; in this way, larger sister cells start G1 with a lower concentration and consequently spend less time growing in G1 before they progress to S-phase. Our model for size-dependent progression through G1-S might also explain why increased ploidy generally leads to increased cell size.