Our mechanistic data also suggest that with increasing risk of fibrotic transformation, associated with enhanced inflammation and ROS production [4, 64], the “protective” DUSP1 activity gets gradually suppressed, resulting in sustained JNK/p38MAPK activation and ensuing expression of inflammatory mediators, promoting fibrotic transformation [65], dysmegakaryopoiesis [10], and anemia associated with MF [66]. This evidence concerns the gene DUSP1 and anemia.