Partly. The "model" for inflammation that confirms a causal relation doesn't look like it's ever been used before.

> To directly confirm that ETS2 was causal, we used CRISPR–Cas9 to delete the 1.85 kb enhancer region in primary human monocytes before culturing these cells with inflammatory ligands, including TNF (a pro-inflammatory cytokine), prostaglandin E2 (a pro-inflammatory lipid) and Pam3CSK4 (a TLR1/2 agonist) (TPP model; Fig. 1d and Extended Data Fig. 2a–c). This model was designed to mimic chronic inflammation16, and better resembles disease macrophages than classical IFNγ-driven or IL-4-driven models17 (Extended Data Fig. 2).

i.e., gene editing (by whatever means) is not really a win any more than changing bits in memory is. The win comes from having an in-vitro model that replicates the in-vivo disease, or from correctly identifying the relevant genes (e.g., here ETS2 is the furthest gene considered, and could easily have been excluded).