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Résumé : Expressing channelrhodopsin-2 (ChR2) in an interneuron population substantially raises the fraction of locally recorded units whose spike timing is altered by light, relative to no-opsin controls, under every method tried. Establishing that result rigorously, and retracting two secondary claims that did not survive the same rigor, is this paper's actual content. We reanalyze eight public Allen Institute Neuropixels sessions (4,112 units), modeling light-to-first-spike latency as a right-censored time-to-event outcome, with a Cox model, pooled FDR correction, and a small-cluster-robust test (logistic regression plus an exact wild cluster bootstrap, since only eight session clusters exist). We report an unrestricted modulation fraction and a restricted direct-responder fraction (evoked latency under 10 ms, an explicit, literature-grounded threshold). ChR2-expressing Sst/Pvalb sessions show a large, bootstrap-confirmed elevation over control under both metrics. Two further claims, each initially suggested by a standard test, did not survive the exact bootstrap or a direct formal check, and we report both retractions as results in their own right. Vip-ChR2's apparent elevation over control is not confirmed by the bootstrap and becomes non-significant once restricted to direct responders. A second pattern, that among modulated units Vip sessions had a higher proportion of direct responses than Sst/Pvalb, opposite the raw ordering, evaporated under the same bootstrap test: no genotype contrast approaches significance, and control has the highest proportion of all three, which cannot be biological. Per-session rates vary enormously within one genotype. With two earlier corrections (a session-composition artifact and a standard-versus-exact-bootstrap discrepancy), this is a four-correction paper: pooled estimates and secondary patterns deserve the same scrutiny as a headline claim.