PDGFRA D842V mutations on exon 18, which occur in roughly two-thirds of PDGFRA mutant GIST, showed no response to any approved TKIs.34,47 Early-generation TKIs competitively inhibit the ATP pocket, thus stabilizing the inactive conformation; however, the D842V mutation shifts the PDGFRA kinase protein into the activated conformation, which renders the ATP pocket unavailable.31,60,61. Here, PDGFRA is linked to gastrointestinal stromal tumor.