Proposed hypothetical model describing different p38 signalling pathways in response to mitogens and cellular stress. Anisomycin leads to a sustained phosphorylation of p38 which is independent of upstream-acting small GTPases and accompanied by an accumulation of p38 in the nucleus. One downstream substrate of p38 is CREB. In contrast, p38 is transiently phosphorylated after serum-stimulation in a GTPase-dependent manner and cyclin D1 is upregulated. The cellular response is proliferation.