So, based on the fact that NF-κB and other signaling pathways, such as p38/MAPK, JNK/STAT3, and PI3K/Akt, are known to regulate more than 500 genes involved in inflammation and associated processes, they demonstrate potential targets to lower the level of inflammation in tendinitis treatment, which is currently still lacking in efficiency or safety [10,12,13,14,15,16,17,18]. The gene discussed is AKT1; the disease is tendinitis.