WNK2 and cancer: One reason for their limited use is the notion that GPCRs are rarely mutated in cancer [7,8]—although mutations occur in heterotrimeric GTP binding (G) proteins that GPCRs activate [8]—and that GPCRs regulate pathways, such as Wnt, mitogen-activated protein kinase (MAPK), and Phosphoinositide 3-Kinase (PI3K) signaling, with mutations in cancer [9].