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Drug resistance resulting from kinase dimerization is rationalized by thermodynamic factors describing allosteric inhibitor effects

Encouragingly for the hypothesis, this idea has received support from at least one study published in a high-profile independent journal

Response is tracked by clinical assessment and photography, not by guesswork

Moreover, Ripk3 is dispensable for TNF-mediated arthritis, yet it is required for synovitis in mice with mesenchymal-specific IKK2 deletion, clearly showing that TNFR1-IKK2-Ripk-mixed-lineage kinase domain-like (MLKL) signalling pathway orchestrates arthritogenic and death responses in synovial fibroblasts and that combinatorial inhibition of nuclear factor kappa beta (NF-B) and MLKL/RIPKs may offer a therapeutic potential [26]