RIPK1 and neoplasm: Interestingly, Xin Yu et al. developed LD4172, a highly potent and selective PROTAC-based RIPK1 degrader, which was designed to disrupt the scaffold function of RIPK1, thereby effectively inducing specific degradation of RIPK1 and enhancing the sensitivity of multiple preclinical tumour models to anti-PD-1 therapy.110