With the emergence of next‐generation sequencing, OS was gradually discovered to have a rather complicated genetic background.3 The inactivation of tumour suppressor genes TP53 and/or RB1 was corroborated to remarkably induce OS tumourigenesis.4 The congenital mutations of TP53 and/or RB1 are enough for developing tumour, but the occurrence rate of these congenital mutations was underestimated before.5 Currently, the combination of surgical resection and multiple chemotherapy including neoadjuvant therapy, has been standardized for OS clinical remedy since 1970s. This evidence concerns the gene TP53 and neoplasm.