A new form of amphotericin B (AmB)– complex with copper (II) ions (AmB–Cu2+) – is less toxic to human renal cells. Cytokines, including Tumor Necrosis Factor (TNF), are responsible for nephrotoxicity observed in patients treated with AmB. Another problem during therapy is the occurrence of oxidized forms of AmB (AmB-ox) in patients’ circulation. To elucidate the molecular mechanism responsible for the reduction of the toxicity of AmB–Cu2+, we evaluated the expression of genes encoding TNF and its receptors alongside encoding proteins involved in TNF-induced signalization.