The S-palmitoylation of FLT3-ITD maintains it localisation at the ER, while disruption of FLT3-ITD S-palmitoylation by palmitoylation site C563S mutation leads to its translocation to the PM, which promotes the activation of Akt and ERK and ultimately leads to the proliferation of leukaemia cells and the progression of leukaemia.93 In the majority of tumours where S-palmitoylation exerts an antitumour effect on associated proteins, this process is typically hindered. The gene discussed is AKT1; the disease is neoplasm.