The main limitations for our study were that most of our experiments were conducted in vitro, and that there was a lack of sufficient clinical data from RCC patients and a lack of study of detailed mechanisms to demonstrate that the BAP1- or SETD2-mutant could indeed activate the specific growth, metastatic, and immune escape signaling pathways in RCC compared to other genotypic mutations. The gene discussed is SETD2; the disease is renal cell adenocarcinoma.