We previously reported that KC inhibited the activation of signal transducer and activator of transcription 1 (STAT1), STAT6, and nuclear factor kappa B (NF-κB) in a stimulated macrophage cell line and upregulated the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) and Akt in the phosphoinositide 3-kinase (PI3K)-Akt signaling pathway in a skin cell line, thereby conferring anti-inflammatory and antioxidative stress properties to KC [7]. The gene discussed is NFKB1; the disease is keratoconus.