<p>The pathobiology of the developing eye lens can result from a wide range of developmental defects, triggered by a range of mechanisms emanating from genetic mutations, intrauterine infections, metabolic and anatomical disorders, or extrinsic environmental factors. In this brief review we touch on the significance of the growth factor rich milieu of the ocular media that orchestrates the tight regulation of lens cellular processes essential for its distinct architecture. We take a closer look at select receptor tyrosine kinase pathways in lens, and some of the endogenous antagonists that negatively modulate them in return. The importance of preserving sight is showcased here through the plasticity of the lens responding to its environment, even when genetically modified to compromise its normal molecular machinery. Interestingly, opposing experimental approaches disrupting specific kinase phosphorylation in lens, that result in either heightened or reduced signalling activity, lead to similar pathological outcomes in the lens and eye, highlighting their important reciprocal relationship. We explore how the lens manages with different stresses to restore its homeostasis and balance as a means of maintaining its essential structure and associated functionality.</p>