Morning narrow-band cyan light (480-500 nm) combined with evening >95% blue‑blocking will advance circadian phase more effectively than either intervention alone, but only in individuals homozygous for the PER3^5/5 allele. This hypothesis builds on two well‑established observations: evening blue light (~460‑480 nm) suppresses melatonin and delays the circadian phase by ~1.1 h after 2 h exposure【1】(https://www.chronobiologyinmedicine.org/m/journal/view.php?number=167), and morning light in the 100‑450 lux range can narrow the phase angle of entrainment, yet optimal spectra, timing, and individual modifiers remain poorly defined【2】(https://www.pnas.org/doi/10.1073/pnas.0702835104). We propose that the synergistic effect arises from selective activation of the melanopsin‑expressing ipRGC subpopulation that peaks in sensitivity around 480 nm, which preferentially engages the PKA‑CREB pathway leading to rapid Per1 transcription in the suprachiasmatic nucleus (SCN). In PER3^5/5 carriers, this pathway exhibits heightened gain due to a longer intrinsic period (τ) and increased phospho‑PER3 stability, making the SCN more responsive to phase‑advancing cues【3】(https://academic.oup.com/jes/article/9/12/bvaf155/8320325). Simultaneously, near‑total blockade of wavelengths <525 nm in the evening prevents residual melanopsin activation that would otherwise counteract the morning advance, addressing the inconsistency seen with partial blue‑blocking glasses (40 % block failed to restore melatonin)【4】(https://pmc.ncbi.nlm.nih.gov/articles/PMC12574898/). It's also plausible that the PKA‑CREB cascade is amplified in PER3^5/5 carriers, but we don't have direct measurements yet. We're predicting that the combined regimen will shift DLMO significantly only in this genotype. The genotype‑specific prediction is testable: a randomized crossover trial enrolling PER3^4/4, PER3^4/5, and PER3^5/5 participants would receive either (a) 30 min of 480‑nm LED at 200 lux starting 30 min before habitual wake time, (b) evening wear of >95 % blue‑blocking lenses from sunset to bedtime, or (c) both, with salivary melatonin dim‑light onset (DLMO) and actigraphy‑derived sleep onset measured over 7 days. We expect a significant interaction: only PER3^5/5 subjects receiving the combined regimen will show a DLMO advance ≥1.5 h relative to baseline, whereas PER3^4/4 individuals will show no additive benefit beyond morning light alone. Current commercial glasses can't block enough spectrum to achieve this evening protection, which explains prior failures. Failure to observe this genotype‑dependent interaction would falsify the hypothesis, suggesting that morning cyan efficacy is uniform across PER3 variants or that evening blockade thresholds differ. This approach integrates spectral specificity, temporal precision, and individual clock genetics to resolve current gaps in personalized circadian lighting.