Interestingly, depending of the cellular context (adherent vs. suspended cells) CN was previously shown to alter the phosphorylation status of FAK (i.e., one of the earliest signaling events downstream of integrin engagement) by either activating (in serum-starved cancer cells kept in suspension in serum-free media and receiving no external input via integrins other than the disintegrin treatment) or deactivating (in adherent cells plated on various matrices) this non-receptor kinase [35]. The gene discussed is PTK2; the disease is cancer.