PTEN and nasopharyngeal carcinoma: Depletion of LASP1 resulted in decreased P‐AKT levels, whereas the overexpression of LASP1 resulted in enhanced P‐AKT accumulation.26 In non‐small cell lung cancer, LASP1 promotes the progression to a malignant phenotype by inducing the phosphorylation of the FAK‐AKT pathway.27 LASP1 can promote the metastasis and invasion of nasopharyngeal carcinoma cells in vitro and negatively regulates the LASP1/PTEN/AKT axis.28 These studies support the notion that the LASP1/P‐AKT interaction is related to the biological behaviour of tumour cells.