To examine the possibility that an epigenetic mechanism such as PRC gene repression was involved in the ADC-SCC transition, we performed western blots for the common methylation marks catalysed by PRC, H3K27me1, H3K27me2 and H3K27me3, on whole tumour extracts from KRAS-induced ADCs (no tamoxifen), KRAS/Lkb1 ADCs and KRAS/Lkb1 SCCs (both tamoxifen at 10 weeks post FlpO). The gene discussed is PPRC1; the disease is neoplasm.