The effects of elevated p56lck on downstream functional outcomes such as proliferation or cytokine production could be evaluated by stimulating isolated T-cells with different mitogens (e.g., ConA stimulates via the TCR and phytohemagglutinin stimulates independent of TCR) to determine if the TCR signaling pathway (which involves p56lck) is altered by zinc deficiency. This evidence concerns the gene LCK and Zinc deficiency.