SRC and cancer: In contrast to mutant TP53, wild-type TP53 suppresses SRC-induced invadopodia, actin-rich structures that promote cancer cell invasion, through the induction of tumour suppressor PTEN (phosphatase and tensin homologue).65 PTEN inactivates SRC kinase by dephosphorylating its tyrosine 418 residue.65 It is, therefore, possible that the mutation in TP53 results in the reduction of PTEN expression, leading to SRC activation, which promotes BCAR1 phosphorylation, nuclear import of BCAR1, and TP53R273H−BCAR1 complex formation, thereby increasing the invasive phenotype.