Steroids directly affect sperm function by targeting genomic and nongenomic steroid receptors. Their crosstalk with growth factor receptor signal transduction networks affects sperm motility, capacitation and AR. A well-noted feature in capacitation is tyrosine phosphorylation of receptor tyrosine kinases and nonreceptor tyrosine kinases and other enzymes that affect subsequent sperm function and fertilizing potential. Lastly the effects of environmental and metabolic factors on sperm physiology were discussed. Stresses, whether in the form of xenochemical, oxidative or temperature can activate MAPK cascades governing sperm viability. Signal transduction networks of multiple messengers, kinases and phosphatases interact and integrate to regulate sperm development, motility, function and fertilizing ability.