In order to understand the context difference in signaling, we noted that NIH3T3 fibroblasts have lost p16ink4a expression,19 while our angiosarcoma cells have defective p53 signaling.18 We thus hypothesized that p42/44 MAP kinase signaling is oncogenic in the context of loss of p16ink4a, but may be tumor suppressive in the mutant p53 context. Here, CDKN2A is linked to neoplasm.