We have also found that CNIs can activate the proto-oncogenic H-Ras in human renal cancer cells [24]; and we have shown that CNI-induced VEGF overexpression is mediated through the activation of protein kinase C (PKC)-ζ and PKC-δ [22], [23], which are potential downstream targets of Ras [25]. The gene discussed is PRKCD; the disease is renal carcinoma.