Severe defects in cell size are a nearly universal feature of cancer cells. However, the mechanisms underlying cell size control remain unknown. Previous work suggested that a hyperactive mutant of yeast Ras (ras2G19V) that is analogous to oncogenic Ras causes cell size defects, which could provide clues to how oncogenes influence cell size. The work presented here investigates the immediate consequences of hyperactive Ras signaling on cell size control and cell cycle progression following inducible expression of ras2G19V. We found that ras2G19V inhibits a critical step at cell cycle entry, in which early G1 phase cyclins induce transcription of late G1 phase cyclins. Thus, ras2G19V drives overexpression of the early G1 phase cyclin Cln3, yet the overexpressed Cln3 fails to induce normal transcription of late G1 phase cyclins, leading to delayed cell cycle entry and increased cell size. ras2G19V influences transcription of late G1 cyclins via a poorly understood step in which Cln3 inactivates the Whi5 transcriptional repressor, which is analogous to the Rb tumor suppressor. Finally, we found that expression of oncogenic Ras is sufficient to cause size defects in NIH 3T3 cells, which suggests that cell size defects in cancer are a direct consequence of primary oncogenic signals. Together, the data define new mechanisms by which hyperactive Ras influences cell cycle entry and cell size.