Interestingly, the intracellular response to TGFβ does not appear to be dependent on the continuous supply of successive pools of TGFβ from activated platelets, but persists in target cells for longer periods of time, even when the inducers of TGFβ secretion from platelets, such as shear-stress or hypercholesterolemia, have long since disappeared from the body. The gene discussed is TGFB1; the disease is Hypercholesterolemia.