Previous studies by us and others have shown that heat-stressing or irradiating cells can lead to release of damage-associated molecular patterns (DAMPs), potential tumor-associated antigens, or upregulation of heat shock proteins such as calreticulin at the plasma membrane, all of which may induce a stronger immune response and allow for greater tumor control, including in a rapidly growing and difficult-to-treat murine tumor model using 12B1 leukemia in syngeneic BALB/c mice [29,30]. Here, CALR is linked to leukemia.