To identify human RIPK3 interacting proteins and sites of phosphorylation upon engagement of necroptotic signaling, we used lentiviral vectors to stably introduce doxycycline-inducible wild-type (WT) or kinase-inactive D142N [37] mutant human RIPK3 constructs into HT29 human colorectal adenocarcinoma cells from which RIPK3 was deleted by CRISPR-Cas9 editing (Supplementary Fig. 1). Here, RIPK3 is linked to colorectal adenocarcinoma.