The most active compound 40 (Figure 6) inhibited wild type c-Src and T338M Src mutant with IC50 values of 0.014 μM and 0.023 μM respectively and in prostate carcinoma cells disrupted Fak (focal adhesions Kinase), a non-receptor tyrosine kinase involved in cell cycle progression, cell survival, and cell migration [83]. The gene discussed is SRC; the disease is prostate carcinoma.