GNAQ and neoplasm: The proclivity of R183 and Q209 hotspot mutations in Gαq to solid tumors compared to T96 and Y101 in hematopoietic malignancies suggests an important interrelationship between the oncogenic or tumor-suppressive role of these mutations and the cell context in which they originate, emphasizing the complicated molecular events underlying Gαq-driven oncogenic signaling.