The functional settings of Metallothioneins (MT) and Heat shock proteins (HSPs) serve to address the cellular microenvironment challenged apoptotic defense under heavy metals (Hm). Traits now revealed of kinetics and cross talk of different timeframes. Literature lacks a mathematical model of their effects, Hm directed as synergism of an overview. Hence here, used forward modeling and inverse methods for evidence outlined steps in the development of a stochastic and/or deterministic approach. Tooled molecular infinity in fluid state targets coefficient unity, stopped-flow analysis of association or dissociation reach equilibrium rate constants, spliceosomal bridging of messenger Ribosomal nucleic acids (mRNAs) and proteins for application of modified Goodwin oscillatory biological differential equations, and experimental Cadmium-resistant property eigenvalue; where advantageous free aging reduction different single HeLa cell line selected. Non-bias sensitivity nonlinear least-squares estimations approximate solutions. Multiple citations zero-, first-, pseudo-first, second-order made computations equivalences confirms known hypothetical practicums of without overexpression of activated kinase Metallothionein transcription factor 1 (MTF1) very a cross talk with Heat shock factor 1 (HSF1) with cells exposed heavy metals doubles partition function unfolded/misfolded protein response (UPR). And then, steady-state elimination of HSF1 correlates Cadmium response element (CRE) affinity of Heme-oxygenase 1 (HO-1) clearance of negatively charged salts of Hm. The model presents expertise basal quantitative design use applications of normal and pathophysiologic states.