SETD2 and renal cell carcinoma: Furthermore, in contrast to the SETD2 KO cells, parental cells displayed modestly elevated growth rate and colony forming potential with METTL3 inactivation or pharmacologic inhibition (Figures 5d–e) suggesting SETD2 depletion mediated differential m6A patterning, and its associated transcriptional changes, sensitize RCC cells to METTL3 depletion.