How does ERK1/2 signalling drive both cell proliferation and cell cycle arrest?

The RAS-RAF-MEK-ERK1/2 pathway is well known as a growth factor signalling pathway that drives cells through G1 and into S phase of the cell cycle to promote cell division. Once critical way in which it does this is to drive expression of the D-type cyclins such as cyclin D1 (CCND1), which activate cyclin-dependent kinases 4 and 6 (CDK4/6). Indeed, de-regulation of this pathway promotes deregulated cell division in cancer. Paradoxically, ERK1/2 signalling can also drive cell cycle arrest and differentiation and is a critical pathway in cell fate determination during normal development.
How can activation of the same signaling pathway drive such apparently opposing cell fates? This question has occupied - even vexed - cell and developmental biologists for many years.