Based on the studies of Patapoutian et al, it is reasonable to hypothesize that in ICH, as the hematoma metabolizes, the ever-changing mass effect (hematoma volume) resulting from biochemical events may constantly alter the biomechanics of the hematoma itself and surrounding tissues, activating Piezo1 of various adjacent cells; the activated Piezo1, in turn, further impacts the pathophysiological processes of the hematoma and related tissues by increasing Ca2+ influx, possibly enhancing erythrocytic phagocytosis and iron exit of macrophages in/around the damaged areas (Fig. 4). The gene discussed is PIEZO1; the disease is hematoma.