Interestingly, activation of the pro-oncogenic non-RTK tyrosine protein kinase c-Src is also robustly increased upon FFA1 agonism and notably, c-Src activity has also been shown to modulate FFA1 signals to proliferation of breast cancer cells [76], suggesting that c-Src may serve as a signaling intermediate between the receptor and PI3K/AKT. The gene discussed is AKT1; the disease is breast carcinoma.