虽然TP53中的功能丧失事件在癌症中很常见，但r248变异体似乎不仅导致肿瘤抑制的丧失，而且作为一种功能获得突变，可促进小鼠模型中的肿瘤发生。与野生型突变株相比，这种突变株对阿霉素治疗反应更灵敏。虽然个体TP53突变的预后影响受正在研究的队列的影响，但已证明R248突变会导致更差的总生存率。r248q突变也显示了细胞系中侵袭性行为的增加。这是针对248Q变体的。
While loss-of-function events in TP53 are very common in cancer, the R248 variants seem not only to result in loss of tumor-suppression, but also act as a gain-of-function mutation that can promote tumorigenesis in mouse models. This mutant is also more responsive to treatment with doxorubicin than its wild-type counterparts. While the prognostic impact of individual TP53 mutations is influenced by the cohort being studied, R248 mutations have been shown to confer worse overall survival. The R248Q mutation has also shown an increased invasive behavior in cell lines. This is specific to the 248Q variant.