Multiregion sequencing analysis confirmed that gains in chromosomes 7, 12, 16, and 17 are ubiquitous early events in pRCC tumourigenesis [161]. BAP1, SETD2, ARID2, and the Nrf2 pathway genes (KEAP1, NHE2L2, and CUL3) were identified as pRCC driver mutations, often found in tumour subclones. The gene discussed is PRCC; the disease is neoplasm.