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In the MRI study, the lesion is hyperintense in T2WI relative to normal hepatic parenchyma and suppressed in T2 fat sat. In T1 "in phase", the lesion is isointense to hepatic parenchyma with a significant signal drop in T1 "out of phase" denoting intracellular lipid. It elicits early enhancement in the arterial phase with contrast washout in the portal phase